Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases

Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced acute tissue injury has been extensively studied, little is known about the role of endothelial cell senescence in the pathogenesis of radiation-...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Yingying Wang [verfasserIn] Marjan Boerma Daohong Zhou

Format:	Artikel
Sprache:	Englisch

Erschienen:	2016

Systematik:	WA 15000

Übergeordnetes Werk:	Enthalten in: Radiation research - Lawrence, Kan. : Soc., 1954, 186(2016), 2, Seite 153-161
Übergeordnetes Werk:	volume:186 ; year:2016 ; number:2 ; pages:153-161

Links:	Volltext Link aufrufen Link aufrufen

DOI / URN:	10.1667/RR14445.1

Katalog-ID:	OLC1981200096

Internformat


LEADER	01000caa a2200265 4500
001	OLC1981200096
003	DE-627
005	20230519005136.0
007	tu
008	161013s2016 xx \|\|\|\|\| 00\| \|\|eng c
024	7		\|a 10.1667/RR14445.1 \|2 doi
028	5	2	\|a PQ20161012
035			\|a (DE-627)OLC1981200096
035			\|a (DE-599)GBVOLC1981200096
035			\|a (PRQ)c1142-b4397ecb7b7dc4f3830614d6e62f2c4181c7867fe9457728d87bb86159aa95bf0
035			\|a (KEY)0012922420160000186000200153ionizingradiationinducedendothelialcellsenescencea
040			\|a DE-627 \|b ger \|c DE-627 \|e rakwb
041			\|a eng
082	0	4	\|a 610 \|a 530 \|q DNB
084			\|a WA 15000 \|q AVZ \|2 rvk
084			\|a 44.64 \|2 bkl
084			\|a 44.40 \|2 bkl
084			\|a 33.30 \|2 bkl
100	0		\|a Yingying Wang \|e verfasserin \|4 aut
245	1	0	\|a Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases
264		1	\|c 2016
336			\|a Text \|b txt \|2 rdacontent
337			\|a ohne Hilfsmittel zu benutzen \|b n \|2 rdamedia
338			\|a Band \|b nc \|2 rdacarrier
520			\|a Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced acute tissue injury has been extensively studied, little is known about the role of endothelial cell senescence in the pathogenesis of radiation-induced late effects. Senescent endothelial cells exhibit decreased production of nitric oxide and expression of thrombomodulin, increased expression of adhesion molecules, elevated production of reactive oxygen species and inflammatory cytokines and an inability to proliferate and form capillary-like structures in vitro. These findings suggest that endothelial cell senescence can lead to endothelial dysfunction by dysregulation of vasodilation and hemostasis, induction of oxidative stress and inflammation and inhibition of angiogenesis, which can potentially contribute to radiation-induced late effects such as cardiovascular diseases (CVDs). In this article, we discuss the mechanisms by which radiation induces endothelial cell senescence, the roles of endothelial cell senescence in radiation-induced CVDs and potential strategies to prevent, mitigate and treat radiation-induced CVDs by targeting senescent endothelial cells.
700	0		\|a Marjan Boerma \|4 oth
700	0		\|a Daohong Zhou \|4 oth
773	0	8	\|i Enthalten in \|t Radiation research \|d Lawrence, Kan. : Soc., 1954 \|g 186(2016), 2, Seite 153-161 \|w (DE-627)129270644 \|w (DE-600)80322-4 \|w (DE-576)01446120X \|x 0033-7587 \|7 nnns
773	1	8	\|g volume:186 \|g year:2016 \|g number:2 \|g pages:153-161
856	4	1	\|u http://dx.doi.org/10.1667/RR14445.1 \|3 Volltext
856	4	2	\|u http://www.ncbi.nlm.nih.gov/pubmed/27387862
856	4	2	\|u http://search.proquest.com/docview/1813038733
912			\|a GBV_USEFLAG_A
912			\|a SYSFLAG_A
912			\|a GBV_OLC
912			\|a SSG-OLC-PHY
912			\|a SSG-OLC-CHE
912			\|a SSG-OLC-PHA
912			\|a SSG-OLC-DE-84
912			\|a SSG-OPC-PHA
912			\|a GBV_ILN_170
912			\|a GBV_ILN_2006
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4219
912			\|a GBV_ILN_4256
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4306
936	r	v	\|a WA 15000
936	b	k	\|a 44.64 \|q AVZ
936	b	k	\|a 44.40 \|q AVZ
936	b	k	\|a 33.30 \|q AVZ
951			\|a AR
952			\|d 186 \|j 2016 \|e 2 \|h 153-161

Indexfelder

author_variant	y w yw
matchkey_str	article:00337587:2016----::oiigaitoidcdnohlaclsnsecada
hierarchy_sort_str	2016
bklnumber	44.64 44.40 33.30
publishDate	2016
allfields	10.1667/RR14445.1 doi PQ20161012 (DE-627)OLC1981200096 (DE-599)GBVOLC1981200096 (PRQ)c1142-b4397ecb7b7dc4f3830614d6e62f2c4181c7867fe9457728d87bb86159aa95bf0 (KEY)0012922420160000186000200153ionizingradiationinducedendothelialcellsenescencea DE-627 ger DE-627 rakwb eng 610 530 DNB WA 15000 AVZ rvk 44.64 bkl 44.40 bkl 33.30 bkl Yingying Wang verfasserin aut Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced acute tissue injury has been extensively studied, little is known about the role of endothelial cell senescence in the pathogenesis of radiation-induced late effects. Senescent endothelial cells exhibit decreased production of nitric oxide and expression of thrombomodulin, increased expression of adhesion molecules, elevated production of reactive oxygen species and inflammatory cytokines and an inability to proliferate and form capillary-like structures in vitro. These findings suggest that endothelial cell senescence can lead to endothelial dysfunction by dysregulation of vasodilation and hemostasis, induction of oxidative stress and inflammation and inhibition of angiogenesis, which can potentially contribute to radiation-induced late effects such as cardiovascular diseases (CVDs). In this article, we discuss the mechanisms by which radiation induces endothelial cell senescence, the roles of endothelial cell senescence in radiation-induced CVDs and potential strategies to prevent, mitigate and treat radiation-induced CVDs by targeting senescent endothelial cells. Marjan Boerma oth Daohong Zhou oth Enthalten in Radiation research Lawrence, Kan. : Soc., 1954 186(2016), 2, Seite 153-161 (DE-627)129270644 (DE-600)80322-4 (DE-576)01446120X 0033-7587 nnns volume:186 year:2016 number:2 pages:153-161 http://dx.doi.org/10.1667/RR14445.1 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27387862 http://search.proquest.com/docview/1813038733 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-PHA GBV_ILN_170 GBV_ILN_2006 GBV_ILN_4112 GBV_ILN_4219 GBV_ILN_4256 GBV_ILN_4305 GBV_ILN_4306 WA 15000 44.64 AVZ 44.40 AVZ 33.30 AVZ AR 186 2016 2 153-161
spelling	10.1667/RR14445.1 doi PQ20161012 (DE-627)OLC1981200096 (DE-599)GBVOLC1981200096 (PRQ)c1142-b4397ecb7b7dc4f3830614d6e62f2c4181c7867fe9457728d87bb86159aa95bf0 (KEY)0012922420160000186000200153ionizingradiationinducedendothelialcellsenescencea DE-627 ger DE-627 rakwb eng 610 530 DNB WA 15000 AVZ rvk 44.64 bkl 44.40 bkl 33.30 bkl Yingying Wang verfasserin aut Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced acute tissue injury has been extensively studied, little is known about the role of endothelial cell senescence in the pathogenesis of radiation-induced late effects. Senescent endothelial cells exhibit decreased production of nitric oxide and expression of thrombomodulin, increased expression of adhesion molecules, elevated production of reactive oxygen species and inflammatory cytokines and an inability to proliferate and form capillary-like structures in vitro. These findings suggest that endothelial cell senescence can lead to endothelial dysfunction by dysregulation of vasodilation and hemostasis, induction of oxidative stress and inflammation and inhibition of angiogenesis, which can potentially contribute to radiation-induced late effects such as cardiovascular diseases (CVDs). In this article, we discuss the mechanisms by which radiation induces endothelial cell senescence, the roles of endothelial cell senescence in radiation-induced CVDs and potential strategies to prevent, mitigate and treat radiation-induced CVDs by targeting senescent endothelial cells. Marjan Boerma oth Daohong Zhou oth Enthalten in Radiation research Lawrence, Kan. : Soc., 1954 186(2016), 2, Seite 153-161 (DE-627)129270644 (DE-600)80322-4 (DE-576)01446120X 0033-7587 nnns volume:186 year:2016 number:2 pages:153-161 http://dx.doi.org/10.1667/RR14445.1 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27387862 http://search.proquest.com/docview/1813038733 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-PHA GBV_ILN_170 GBV_ILN_2006 GBV_ILN_4112 GBV_ILN_4219 GBV_ILN_4256 GBV_ILN_4305 GBV_ILN_4306 WA 15000 44.64 AVZ 44.40 AVZ 33.30 AVZ AR 186 2016 2 153-161
allfields_unstemmed	10.1667/RR14445.1 doi PQ20161012 (DE-627)OLC1981200096 (DE-599)GBVOLC1981200096 (PRQ)c1142-b4397ecb7b7dc4f3830614d6e62f2c4181c7867fe9457728d87bb86159aa95bf0 (KEY)0012922420160000186000200153ionizingradiationinducedendothelialcellsenescencea DE-627 ger DE-627 rakwb eng 610 530 DNB WA 15000 AVZ rvk 44.64 bkl 44.40 bkl 33.30 bkl Yingying Wang verfasserin aut Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced acute tissue injury has been extensively studied, little is known about the role of endothelial cell senescence in the pathogenesis of radiation-induced late effects. Senescent endothelial cells exhibit decreased production of nitric oxide and expression of thrombomodulin, increased expression of adhesion molecules, elevated production of reactive oxygen species and inflammatory cytokines and an inability to proliferate and form capillary-like structures in vitro. These findings suggest that endothelial cell senescence can lead to endothelial dysfunction by dysregulation of vasodilation and hemostasis, induction of oxidative stress and inflammation and inhibition of angiogenesis, which can potentially contribute to radiation-induced late effects such as cardiovascular diseases (CVDs). In this article, we discuss the mechanisms by which radiation induces endothelial cell senescence, the roles of endothelial cell senescence in radiation-induced CVDs and potential strategies to prevent, mitigate and treat radiation-induced CVDs by targeting senescent endothelial cells. Marjan Boerma oth Daohong Zhou oth Enthalten in Radiation research Lawrence, Kan. : Soc., 1954 186(2016), 2, Seite 153-161 (DE-627)129270644 (DE-600)80322-4 (DE-576)01446120X 0033-7587 nnns volume:186 year:2016 number:2 pages:153-161 http://dx.doi.org/10.1667/RR14445.1 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27387862 http://search.proquest.com/docview/1813038733 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-PHA GBV_ILN_170 GBV_ILN_2006 GBV_ILN_4112 GBV_ILN_4219 GBV_ILN_4256 GBV_ILN_4305 GBV_ILN_4306 WA 15000 44.64 AVZ 44.40 AVZ 33.30 AVZ AR 186 2016 2 153-161
allfieldsGer	10.1667/RR14445.1 doi PQ20161012 (DE-627)OLC1981200096 (DE-599)GBVOLC1981200096 (PRQ)c1142-b4397ecb7b7dc4f3830614d6e62f2c4181c7867fe9457728d87bb86159aa95bf0 (KEY)0012922420160000186000200153ionizingradiationinducedendothelialcellsenescencea DE-627 ger DE-627 rakwb eng 610 530 DNB WA 15000 AVZ rvk 44.64 bkl 44.40 bkl 33.30 bkl Yingying Wang verfasserin aut Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced acute tissue injury has been extensively studied, little is known about the role of endothelial cell senescence in the pathogenesis of radiation-induced late effects. Senescent endothelial cells exhibit decreased production of nitric oxide and expression of thrombomodulin, increased expression of adhesion molecules, elevated production of reactive oxygen species and inflammatory cytokines and an inability to proliferate and form capillary-like structures in vitro. These findings suggest that endothelial cell senescence can lead to endothelial dysfunction by dysregulation of vasodilation and hemostasis, induction of oxidative stress and inflammation and inhibition of angiogenesis, which can potentially contribute to radiation-induced late effects such as cardiovascular diseases (CVDs). In this article, we discuss the mechanisms by which radiation induces endothelial cell senescence, the roles of endothelial cell senescence in radiation-induced CVDs and potential strategies to prevent, mitigate and treat radiation-induced CVDs by targeting senescent endothelial cells. Marjan Boerma oth Daohong Zhou oth Enthalten in Radiation research Lawrence, Kan. : Soc., 1954 186(2016), 2, Seite 153-161 (DE-627)129270644 (DE-600)80322-4 (DE-576)01446120X 0033-7587 nnns volume:186 year:2016 number:2 pages:153-161 http://dx.doi.org/10.1667/RR14445.1 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27387862 http://search.proquest.com/docview/1813038733 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-PHA GBV_ILN_170 GBV_ILN_2006 GBV_ILN_4112 GBV_ILN_4219 GBV_ILN_4256 GBV_ILN_4305 GBV_ILN_4306 WA 15000 44.64 AVZ 44.40 AVZ 33.30 AVZ AR 186 2016 2 153-161
allfieldsSound	10.1667/RR14445.1 doi PQ20161012 (DE-627)OLC1981200096 (DE-599)GBVOLC1981200096 (PRQ)c1142-b4397ecb7b7dc4f3830614d6e62f2c4181c7867fe9457728d87bb86159aa95bf0 (KEY)0012922420160000186000200153ionizingradiationinducedendothelialcellsenescencea DE-627 ger DE-627 rakwb eng 610 530 DNB WA 15000 AVZ rvk 44.64 bkl 44.40 bkl 33.30 bkl Yingying Wang verfasserin aut Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced acute tissue injury has been extensively studied, little is known about the role of endothelial cell senescence in the pathogenesis of radiation-induced late effects. Senescent endothelial cells exhibit decreased production of nitric oxide and expression of thrombomodulin, increased expression of adhesion molecules, elevated production of reactive oxygen species and inflammatory cytokines and an inability to proliferate and form capillary-like structures in vitro. These findings suggest that endothelial cell senescence can lead to endothelial dysfunction by dysregulation of vasodilation and hemostasis, induction of oxidative stress and inflammation and inhibition of angiogenesis, which can potentially contribute to radiation-induced late effects such as cardiovascular diseases (CVDs). In this article, we discuss the mechanisms by which radiation induces endothelial cell senescence, the roles of endothelial cell senescence in radiation-induced CVDs and potential strategies to prevent, mitigate and treat radiation-induced CVDs by targeting senescent endothelial cells. Marjan Boerma oth Daohong Zhou oth Enthalten in Radiation research Lawrence, Kan. : Soc., 1954 186(2016), 2, Seite 153-161 (DE-627)129270644 (DE-600)80322-4 (DE-576)01446120X 0033-7587 nnns volume:186 year:2016 number:2 pages:153-161 http://dx.doi.org/10.1667/RR14445.1 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27387862 http://search.proquest.com/docview/1813038733 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-PHA GBV_ILN_170 GBV_ILN_2006 GBV_ILN_4112 GBV_ILN_4219 GBV_ILN_4256 GBV_ILN_4305 GBV_ILN_4306 WA 15000 44.64 AVZ 44.40 AVZ 33.30 AVZ AR 186 2016 2 153-161
language	English
source	Enthalten in Radiation research 186(2016), 2, Seite 153-161 volume:186 year:2016 number:2 pages:153-161
sourceStr	Enthalten in Radiation research 186(2016), 2, Seite 153-161 volume:186 year:2016 number:2 pages:153-161
format_phy_str_mv	Article
institution	findex.gbv.de
dewey-raw	610
isfreeaccess_bool	false
container_title	Radiation research
authorswithroles_txt_mv	Yingying Wang @@aut@@ Marjan Boerma @@oth@@ Daohong Zhou @@oth@@
publishDateDaySort_date	2016-01-01T00:00:00Z
hierarchy_top_id	129270644
dewey-sort	3610
id	OLC1981200096
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a2200265 4500</leader><controlfield tag="001">OLC1981200096</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519005136.0</controlfield><controlfield tag="007">tu</controlfield><controlfield tag="008">161013s2016 xx \|\|\|\|\| 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1667/RR14445.1</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">PQ20161012</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)OLC1981200096</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)GBVOLC1981200096</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(PRQ)c1142-b4397ecb7b7dc4f3830614d6e62f2c4181c7867fe9457728d87bb86159aa95bf0</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(KEY)0012922420160000186000200153ionizingradiationinducedendothelialcellsenescencea</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="a">530</subfield><subfield code="q">DNB</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">WA 15000</subfield><subfield code="q">AVZ</subfield><subfield code="2">rvk</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.64</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.40</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">33.30</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Yingying Wang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">ohne Hilfsmittel zu benutzen</subfield><subfield code="b">n</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Band</subfield><subfield code="b">nc</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced acute tissue injury has been extensively studied, little is known about the role of endothelial cell senescence in the pathogenesis of radiation-induced late effects. Senescent endothelial cells exhibit decreased production of nitric oxide and expression of thrombomodulin, increased expression of adhesion molecules, elevated production of reactive oxygen species and inflammatory cytokines and an inability to proliferate and form capillary-like structures in vitro. These findings suggest that endothelial cell senescence can lead to endothelial dysfunction by dysregulation of vasodilation and hemostasis, induction of oxidative stress and inflammation and inhibition of angiogenesis, which can potentially contribute to radiation-induced late effects such as cardiovascular diseases (CVDs). In this article, we discuss the mechanisms by which radiation induces endothelial cell senescence, the roles of endothelial cell senescence in radiation-induced CVDs and potential strategies to prevent, mitigate and treat radiation-induced CVDs by targeting senescent endothelial cells.</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Marjan Boerma</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Daohong Zhou</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Radiation research</subfield><subfield code="d">Lawrence, Kan. : Soc., 1954</subfield><subfield code="g">186(2016), 2, Seite 153-161</subfield><subfield code="w">(DE-627)129270644</subfield><subfield code="w">(DE-600)80322-4</subfield><subfield code="w">(DE-576)01446120X</subfield><subfield code="x">0033-7587</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:186</subfield><subfield code="g">year:2016</subfield><subfield code="g">number:2</subfield><subfield code="g">pages:153-161</subfield></datafield><datafield tag="856" ind1="4" ind2="1"><subfield code="u">http://dx.doi.org/10.1667/RR14445.1</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://www.ncbi.nlm.nih.gov/pubmed/27387862</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://search.proquest.com/docview/1813038733</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_OLC</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHY</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-CHE</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-DE-84</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2006</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4219</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4256</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="936" ind1="r" ind2="v"><subfield code="a">WA 15000</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.64</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.40</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">33.30</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">186</subfield><subfield code="j">2016</subfield><subfield code="e">2</subfield><subfield code="h">153-161</subfield></datafield></record></collection>
author	Yingying Wang
spellingShingle	Yingying Wang ddc 610 rvk WA 15000 bkl 44.64 bkl 44.40 bkl 33.30 Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases
authorStr	Yingying Wang
ppnlink_with_tag_str_mv	@@773@@(DE-627)129270644
format	Article
dewey-ones	610 - Medicine & health 530 - Physics
delete_txt_mv	keep
author_role	aut
collection	OLC
remote_str	false
illustrated	Not Illustrated
issn	0033-7587
topic_title	610 530 DNB WA 15000 AVZ rvk 44.64 bkl 44.40 bkl 33.30 bkl Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases
topic	ddc 610 rvk WA 15000 bkl 44.64 bkl 44.40 bkl 33.30
topic_unstemmed	ddc 610 rvk WA 15000 bkl 44.64 bkl 44.40 bkl 33.30
topic_browse	ddc 610 rvk WA 15000 bkl 44.64 bkl 44.40 bkl 33.30
format_facet	Aufsätze Gedruckte Aufsätze
format_main_str_mv	Text Zeitschrift/Artikel
carriertype_str_mv	nc
author2_variant	m b mb d z dz
hierarchy_parent_title	Radiation research
hierarchy_parent_id	129270644
dewey-tens	610 - Medicine & health 530 - Physics
hierarchy_top_title	Radiation research
isfreeaccess_txt	false
familylinks_str_mv	(DE-627)129270644 (DE-600)80322-4 (DE-576)01446120X
title	Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases
ctrlnum	(DE-627)OLC1981200096 (DE-599)GBVOLC1981200096 (PRQ)c1142-b4397ecb7b7dc4f3830614d6e62f2c4181c7867fe9457728d87bb86159aa95bf0 (KEY)0012922420160000186000200153ionizingradiationinducedendothelialcellsenescencea
title_full	Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases
author_sort	Yingying Wang
journal	Radiation research
journalStr	Radiation research
lang_code	eng
isOA_bool	false
dewey-hundreds	600 - Technology 500 - Science
recordtype	marc
publishDateSort	2016
contenttype_str_mv	txt
container_start_page	153
author_browse	Yingying Wang
container_volume	186
class	610 530 DNB WA 15000 AVZ rvk 44.64 bkl 44.40 bkl 33.30 bkl
format_se	Aufsätze
author-letter	Yingying Wang
doi_str_mv	10.1667/RR14445.1
dewey-full	610 530
title_sort	ionizing radiation-induced endothelial cell senescence and cardiovascular diseases
title_auth	Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases
abstract	Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced acute tissue injury has been extensively studied, little is known about the role of endothelial cell senescence in the pathogenesis of radiation-induced late effects. Senescent endothelial cells exhibit decreased production of nitric oxide and expression of thrombomodulin, increased expression of adhesion molecules, elevated production of reactive oxygen species and inflammatory cytokines and an inability to proliferate and form capillary-like structures in vitro. These findings suggest that endothelial cell senescence can lead to endothelial dysfunction by dysregulation of vasodilation and hemostasis, induction of oxidative stress and inflammation and inhibition of angiogenesis, which can potentially contribute to radiation-induced late effects such as cardiovascular diseases (CVDs). In this article, we discuss the mechanisms by which radiation induces endothelial cell senescence, the roles of endothelial cell senescence in radiation-induced CVDs and potential strategies to prevent, mitigate and treat radiation-induced CVDs by targeting senescent endothelial cells.
abstractGer	Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced acute tissue injury has been extensively studied, little is known about the role of endothelial cell senescence in the pathogenesis of radiation-induced late effects. Senescent endothelial cells exhibit decreased production of nitric oxide and expression of thrombomodulin, increased expression of adhesion molecules, elevated production of reactive oxygen species and inflammatory cytokines and an inability to proliferate and form capillary-like structures in vitro. These findings suggest that endothelial cell senescence can lead to endothelial dysfunction by dysregulation of vasodilation and hemostasis, induction of oxidative stress and inflammation and inhibition of angiogenesis, which can potentially contribute to radiation-induced late effects such as cardiovascular diseases (CVDs). In this article, we discuss the mechanisms by which radiation induces endothelial cell senescence, the roles of endothelial cell senescence in radiation-induced CVDs and potential strategies to prevent, mitigate and treat radiation-induced CVDs by targeting senescent endothelial cells.
abstract_unstemmed	Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced acute tissue injury has been extensively studied, little is known about the role of endothelial cell senescence in the pathogenesis of radiation-induced late effects. Senescent endothelial cells exhibit decreased production of nitric oxide and expression of thrombomodulin, increased expression of adhesion molecules, elevated production of reactive oxygen species and inflammatory cytokines and an inability to proliferate and form capillary-like structures in vitro. These findings suggest that endothelial cell senescence can lead to endothelial dysfunction by dysregulation of vasodilation and hemostasis, induction of oxidative stress and inflammation and inhibition of angiogenesis, which can potentially contribute to radiation-induced late effects such as cardiovascular diseases (CVDs). In this article, we discuss the mechanisms by which radiation induces endothelial cell senescence, the roles of endothelial cell senescence in radiation-induced CVDs and potential strategies to prevent, mitigate and treat radiation-induced CVDs by targeting senescent endothelial cells.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-PHA GBV_ILN_170 GBV_ILN_2006 GBV_ILN_4112 GBV_ILN_4219 GBV_ILN_4256 GBV_ILN_4305 GBV_ILN_4306
container_issue	2
title_short	Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases
url	http://dx.doi.org/10.1667/RR14445.1 http://www.ncbi.nlm.nih.gov/pubmed/27387862 http://search.proquest.com/docview/1813038733
remote_bool	false
author2	Marjan Boerma Daohong Zhou
author2Str	Marjan Boerma Daohong Zhou
ppnlink	129270644
mediatype_str_mv	n
isOA_txt	false
hochschulschrift_bool	false
author2_role	oth oth
doi_str	10.1667/RR14445.1
up_date	2024-07-04T04:27:22.281Z
_version_	1803621228648333312
fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a2200265 4500</leader><controlfield tag="001">OLC1981200096</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519005136.0</controlfield><controlfield tag="007">tu</controlfield><controlfield tag="008">161013s2016 xx \|\|\|\|\| 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1667/RR14445.1</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">PQ20161012</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)OLC1981200096</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)GBVOLC1981200096</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(PRQ)c1142-b4397ecb7b7dc4f3830614d6e62f2c4181c7867fe9457728d87bb86159aa95bf0</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(KEY)0012922420160000186000200153ionizingradiationinducedendothelialcellsenescencea</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="a">530</subfield><subfield code="q">DNB</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">WA 15000</subfield><subfield code="q">AVZ</subfield><subfield code="2">rvk</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.64</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.40</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">33.30</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Yingying Wang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">ohne Hilfsmittel zu benutzen</subfield><subfield code="b">n</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Band</subfield><subfield code="b">nc</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced acute tissue injury has been extensively studied, little is known about the role of endothelial cell senescence in the pathogenesis of radiation-induced late effects. Senescent endothelial cells exhibit decreased production of nitric oxide and expression of thrombomodulin, increased expression of adhesion molecules, elevated production of reactive oxygen species and inflammatory cytokines and an inability to proliferate and form capillary-like structures in vitro. These findings suggest that endothelial cell senescence can lead to endothelial dysfunction by dysregulation of vasodilation and hemostasis, induction of oxidative stress and inflammation and inhibition of angiogenesis, which can potentially contribute to radiation-induced late effects such as cardiovascular diseases (CVDs). In this article, we discuss the mechanisms by which radiation induces endothelial cell senescence, the roles of endothelial cell senescence in radiation-induced CVDs and potential strategies to prevent, mitigate and treat radiation-induced CVDs by targeting senescent endothelial cells.</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Marjan Boerma</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Daohong Zhou</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Radiation research</subfield><subfield code="d">Lawrence, Kan. : Soc., 1954</subfield><subfield code="g">186(2016), 2, Seite 153-161</subfield><subfield code="w">(DE-627)129270644</subfield><subfield code="w">(DE-600)80322-4</subfield><subfield code="w">(DE-576)01446120X</subfield><subfield code="x">0033-7587</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:186</subfield><subfield code="g">year:2016</subfield><subfield code="g">number:2</subfield><subfield code="g">pages:153-161</subfield></datafield><datafield tag="856" ind1="4" ind2="1"><subfield code="u">http://dx.doi.org/10.1667/RR14445.1</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://www.ncbi.nlm.nih.gov/pubmed/27387862</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://search.proquest.com/docview/1813038733</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_OLC</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHY</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-CHE</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-DE-84</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2006</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4219</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4256</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="936" ind1="r" ind2="v"><subfield code="a">WA 15000</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.64</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.40</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">33.30</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">186</subfield><subfield code="j">2016</subfield><subfield code="e">2</subfield><subfield code="h">153-161</subfield></datafield></record></collection>
score	7.4007626

Nicht das Richtige dabei?

Schreiben Sie uns!

Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases

Nicht das Richtige dabei?

Zugang & Verfügbarkeit

Vorhandene Bände

Nicht das Richtige dabei?