Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation

Patients with end-stage renal failure depend on hemodialysis indefinitely without renal transplantation, requiring a long-term patent vascular access. Although an arteriovenous fistula (AVF) remains the preferred vascular access for hemodialysis because of its longer patency and fewer complications compared with other vascular accesses, the primary patency of AVF is only 50% to 60%, presenting a clinical need for improvement. AVF mature by developing a thickened vascular wall and increased diameter to adapt to arterial blood pressure and flow volume. Inflammation plays a critical role during vascular remodeling and fistula maturation; increased shear stress triggers infiltration of T cells and macrophages that initiate inflammation, with involvement of several different subsets of T cells and macrophages. We review the literature describing distinct roles of the various subsets of T cells and macrophages during vascular remodeling. Immunosuppression with sirolimus or prednisolone decreases neointimal hyperplasia during AVF maturation, suggesting novel approaches to enhance vascular remodeling. However, M2 macrophages and CD4+ T cells play essential roles during AVF maturation, suggesting that total immunosuppression may suppress adaptive vascular remodeling. Therefore, it is likely that regulation of inflammation during fistula maturation will require a balanced approach to coordinate the various inflammatory cell subsets. Advances in immunosuppressive drug development and delivery systems may allow for more targeted regulation of inflammation to improve vascular remodeling and enhance AVF maturation. (JVS–Vascular Science 2020;1:207-18.) : Clinical Relevance: Patients with end-stage renal failure depend on successful AVF maturation to have a useful access. Inflammation occurs during fistula maturation and may be a therapeutic target to improve fistula maturation and utilization. Inflammation is mainly caused by T cells and macrophages, which have several subsets with distinct phenotypes and roles during vascular remodeling. Regulation of inflammation during fistula maturation requires a balanced approach to coordinate the various inflammatory cell subsets. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Yutaka Matsubara, MD, PhD [verfasserIn] Gathe Kiwan, MS [verfasserIn] Arash Fereydooni, MD [verfasserIn] John Langford, MD [verfasserIn] Alan Dardik, MD, PhD [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Arteriovenous fistula Inflammation T-cells Macrophages Vascular remodeling

Übergeordnetes Werk:	In: JVS - Vascular Science - Elsevier, 2021, 1(2020), Seite 207-218
Übergeordnetes Werk:	volume:1 ; year:2020 ; pages:207-218

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.jvssci.2020.07.005

Katalog-ID:	DOAJ070539480

Internformat


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spelling	10.1016/j.jvssci.2020.07.005 doi (DE-627)DOAJ070539480 (DE-599)DOAJ612afa44646f40e6a75ab2adb622ce40 DE-627 ger DE-627 rakwb eng RC666-701 Yutaka Matsubara, MD, PhD verfasserin aut Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Patients with end-stage renal failure depend on hemodialysis indefinitely without renal transplantation, requiring a long-term patent vascular access. Although an arteriovenous fistula (AVF) remains the preferred vascular access for hemodialysis because of its longer patency and fewer complications compared with other vascular accesses, the primary patency of AVF is only 50% to 60%, presenting a clinical need for improvement. AVF mature by developing a thickened vascular wall and increased diameter to adapt to arterial blood pressure and flow volume. Inflammation plays a critical role during vascular remodeling and fistula maturation; increased shear stress triggers infiltration of T cells and macrophages that initiate inflammation, with involvement of several different subsets of T cells and macrophages. We review the literature describing distinct roles of the various subsets of T cells and macrophages during vascular remodeling. Immunosuppression with sirolimus or prednisolone decreases neointimal hyperplasia during AVF maturation, suggesting novel approaches to enhance vascular remodeling. However, M2 macrophages and CD4+ T cells play essential roles during AVF maturation, suggesting that total immunosuppression may suppress adaptive vascular remodeling. Therefore, it is likely that regulation of inflammation during fistula maturation will require a balanced approach to coordinate the various inflammatory cell subsets. Advances in immunosuppressive drug development and delivery systems may allow for more targeted regulation of inflammation to improve vascular remodeling and enhance AVF maturation. (JVS–Vascular Science 2020;1:207-18.) : Clinical Relevance: Patients with end-stage renal failure depend on successful AVF maturation to have a useful access. Inflammation occurs during fistula maturation and may be a therapeutic target to improve fistula maturation and utilization. Inflammation is mainly caused by T cells and macrophages, which have several subsets with distinct phenotypes and roles during vascular remodeling. Regulation of inflammation during fistula maturation requires a balanced approach to coordinate the various inflammatory cell subsets. Arteriovenous fistula Inflammation T-cells Macrophages Vascular remodeling Diseases of the circulatory (Cardiovascular) system Gathe Kiwan, MS verfasserin aut Arash Fereydooni, MD verfasserin aut John Langford, MD verfasserin aut Alan Dardik, MD, PhD verfasserin aut In JVS - Vascular Science Elsevier, 2021 1(2020), Seite 207-218 (DE-627)1755580096 26663503 nnns volume:1 year:2020 pages:207-218 https://doi.org/10.1016/j.jvssci.2020.07.005 kostenfrei https://doaj.org/article/612afa44646f40e6a75ab2adb622ce40 kostenfrei http://www.sciencedirect.com/science/article/pii/S2666350320300171 kostenfrei https://doaj.org/toc/2666-3503 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 1 2020 207-218
allfields_unstemmed	10.1016/j.jvssci.2020.07.005 doi (DE-627)DOAJ070539480 (DE-599)DOAJ612afa44646f40e6a75ab2adb622ce40 DE-627 ger DE-627 rakwb eng RC666-701 Yutaka Matsubara, MD, PhD verfasserin aut Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Patients with end-stage renal failure depend on hemodialysis indefinitely without renal transplantation, requiring a long-term patent vascular access. Although an arteriovenous fistula (AVF) remains the preferred vascular access for hemodialysis because of its longer patency and fewer complications compared with other vascular accesses, the primary patency of AVF is only 50% to 60%, presenting a clinical need for improvement. AVF mature by developing a thickened vascular wall and increased diameter to adapt to arterial blood pressure and flow volume. Inflammation plays a critical role during vascular remodeling and fistula maturation; increased shear stress triggers infiltration of T cells and macrophages that initiate inflammation, with involvement of several different subsets of T cells and macrophages. We review the literature describing distinct roles of the various subsets of T cells and macrophages during vascular remodeling. Immunosuppression with sirolimus or prednisolone decreases neointimal hyperplasia during AVF maturation, suggesting novel approaches to enhance vascular remodeling. However, M2 macrophages and CD4+ T cells play essential roles during AVF maturation, suggesting that total immunosuppression may suppress adaptive vascular remodeling. Therefore, it is likely that regulation of inflammation during fistula maturation will require a balanced approach to coordinate the various inflammatory cell subsets. Advances in immunosuppressive drug development and delivery systems may allow for more targeted regulation of inflammation to improve vascular remodeling and enhance AVF maturation. (JVS–Vascular Science 2020;1:207-18.) : Clinical Relevance: Patients with end-stage renal failure depend on successful AVF maturation to have a useful access. Inflammation occurs during fistula maturation and may be a therapeutic target to improve fistula maturation and utilization. Inflammation is mainly caused by T cells and macrophages, which have several subsets with distinct phenotypes and roles during vascular remodeling. Regulation of inflammation during fistula maturation requires a balanced approach to coordinate the various inflammatory cell subsets. Arteriovenous fistula Inflammation T-cells Macrophages Vascular remodeling Diseases of the circulatory (Cardiovascular) system Gathe Kiwan, MS verfasserin aut Arash Fereydooni, MD verfasserin aut John Langford, MD verfasserin aut Alan Dardik, MD, PhD verfasserin aut In JVS - Vascular Science Elsevier, 2021 1(2020), Seite 207-218 (DE-627)1755580096 26663503 nnns volume:1 year:2020 pages:207-218 https://doi.org/10.1016/j.jvssci.2020.07.005 kostenfrei https://doaj.org/article/612afa44646f40e6a75ab2adb622ce40 kostenfrei http://www.sciencedirect.com/science/article/pii/S2666350320300171 kostenfrei https://doaj.org/toc/2666-3503 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 1 2020 207-218
allfieldsGer	10.1016/j.jvssci.2020.07.005 doi (DE-627)DOAJ070539480 (DE-599)DOAJ612afa44646f40e6a75ab2adb622ce40 DE-627 ger DE-627 rakwb eng RC666-701 Yutaka Matsubara, MD, PhD verfasserin aut Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Patients with end-stage renal failure depend on hemodialysis indefinitely without renal transplantation, requiring a long-term patent vascular access. Although an arteriovenous fistula (AVF) remains the preferred vascular access for hemodialysis because of its longer patency and fewer complications compared with other vascular accesses, the primary patency of AVF is only 50% to 60%, presenting a clinical need for improvement. AVF mature by developing a thickened vascular wall and increased diameter to adapt to arterial blood pressure and flow volume. Inflammation plays a critical role during vascular remodeling and fistula maturation; increased shear stress triggers infiltration of T cells and macrophages that initiate inflammation, with involvement of several different subsets of T cells and macrophages. We review the literature describing distinct roles of the various subsets of T cells and macrophages during vascular remodeling. Immunosuppression with sirolimus or prednisolone decreases neointimal hyperplasia during AVF maturation, suggesting novel approaches to enhance vascular remodeling. However, M2 macrophages and CD4+ T cells play essential roles during AVF maturation, suggesting that total immunosuppression may suppress adaptive vascular remodeling. Therefore, it is likely that regulation of inflammation during fistula maturation will require a balanced approach to coordinate the various inflammatory cell subsets. Advances in immunosuppressive drug development and delivery systems may allow for more targeted regulation of inflammation to improve vascular remodeling and enhance AVF maturation. (JVS–Vascular Science 2020;1:207-18.) : Clinical Relevance: Patients with end-stage renal failure depend on successful AVF maturation to have a useful access. Inflammation occurs during fistula maturation and may be a therapeutic target to improve fistula maturation and utilization. Inflammation is mainly caused by T cells and macrophages, which have several subsets with distinct phenotypes and roles during vascular remodeling. Regulation of inflammation during fistula maturation requires a balanced approach to coordinate the various inflammatory cell subsets. Arteriovenous fistula Inflammation T-cells Macrophages Vascular remodeling Diseases of the circulatory (Cardiovascular) system Gathe Kiwan, MS verfasserin aut Arash Fereydooni, MD verfasserin aut John Langford, MD verfasserin aut Alan Dardik, MD, PhD verfasserin aut In JVS - Vascular Science Elsevier, 2021 1(2020), Seite 207-218 (DE-627)1755580096 26663503 nnns volume:1 year:2020 pages:207-218 https://doi.org/10.1016/j.jvssci.2020.07.005 kostenfrei https://doaj.org/article/612afa44646f40e6a75ab2adb622ce40 kostenfrei http://www.sciencedirect.com/science/article/pii/S2666350320300171 kostenfrei https://doaj.org/toc/2666-3503 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 1 2020 207-218
allfieldsSound	10.1016/j.jvssci.2020.07.005 doi (DE-627)DOAJ070539480 (DE-599)DOAJ612afa44646f40e6a75ab2adb622ce40 DE-627 ger DE-627 rakwb eng RC666-701 Yutaka Matsubara, MD, PhD verfasserin aut Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Patients with end-stage renal failure depend on hemodialysis indefinitely without renal transplantation, requiring a long-term patent vascular access. Although an arteriovenous fistula (AVF) remains the preferred vascular access for hemodialysis because of its longer patency and fewer complications compared with other vascular accesses, the primary patency of AVF is only 50% to 60%, presenting a clinical need for improvement. AVF mature by developing a thickened vascular wall and increased diameter to adapt to arterial blood pressure and flow volume. Inflammation plays a critical role during vascular remodeling and fistula maturation; increased shear stress triggers infiltration of T cells and macrophages that initiate inflammation, with involvement of several different subsets of T cells and macrophages. We review the literature describing distinct roles of the various subsets of T cells and macrophages during vascular remodeling. Immunosuppression with sirolimus or prednisolone decreases neointimal hyperplasia during AVF maturation, suggesting novel approaches to enhance vascular remodeling. However, M2 macrophages and CD4+ T cells play essential roles during AVF maturation, suggesting that total immunosuppression may suppress adaptive vascular remodeling. Therefore, it is likely that regulation of inflammation during fistula maturation will require a balanced approach to coordinate the various inflammatory cell subsets. Advances in immunosuppressive drug development and delivery systems may allow for more targeted regulation of inflammation to improve vascular remodeling and enhance AVF maturation. (JVS–Vascular Science 2020;1:207-18.) : Clinical Relevance: Patients with end-stage renal failure depend on successful AVF maturation to have a useful access. Inflammation occurs during fistula maturation and may be a therapeutic target to improve fistula maturation and utilization. Inflammation is mainly caused by T cells and macrophages, which have several subsets with distinct phenotypes and roles during vascular remodeling. Regulation of inflammation during fistula maturation requires a balanced approach to coordinate the various inflammatory cell subsets. Arteriovenous fistula Inflammation T-cells Macrophages Vascular remodeling Diseases of the circulatory (Cardiovascular) system Gathe Kiwan, MS verfasserin aut Arash Fereydooni, MD verfasserin aut John Langford, MD verfasserin aut Alan Dardik, MD, PhD verfasserin aut In JVS - Vascular Science Elsevier, 2021 1(2020), Seite 207-218 (DE-627)1755580096 26663503 nnns volume:1 year:2020 pages:207-218 https://doi.org/10.1016/j.jvssci.2020.07.005 kostenfrei https://doaj.org/article/612afa44646f40e6a75ab2adb622ce40 kostenfrei http://www.sciencedirect.com/science/article/pii/S2666350320300171 kostenfrei https://doaj.org/toc/2666-3503 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 1 2020 207-218
language	English
source	In JVS - Vascular Science 1(2020), Seite 207-218 volume:1 year:2020 pages:207-218
sourceStr	In JVS - Vascular Science 1(2020), Seite 207-218 volume:1 year:2020 pages:207-218
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Arteriovenous fistula Inflammation T-cells Macrophages Vascular remodeling Diseases of the circulatory (Cardiovascular) system
isfreeaccess_bool	true
container_title	JVS - Vascular Science
authorswithroles_txt_mv	Yutaka Matsubara, MD, PhD @@aut@@ Gathe Kiwan, MS @@aut@@ Arash Fereydooni, MD @@aut@@ John Langford, MD @@aut@@ Alan Dardik, MD, PhD @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	1755580096
id	DOAJ070539480
language_de	englisch
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Although an arteriovenous fistula (AVF) remains the preferred vascular access for hemodialysis because of its longer patency and fewer complications compared with other vascular accesses, the primary patency of AVF is only 50% to 60%, presenting a clinical need for improvement. AVF mature by developing a thickened vascular wall and increased diameter to adapt to arterial blood pressure and flow volume. Inflammation plays a critical role during vascular remodeling and fistula maturation; increased shear stress triggers infiltration of T cells and macrophages that initiate inflammation, with involvement of several different subsets of T cells and macrophages. We review the literature describing distinct roles of the various subsets of T cells and macrophages during vascular remodeling. Immunosuppression with sirolimus or prednisolone decreases neointimal hyperplasia during AVF maturation, suggesting novel approaches to enhance vascular remodeling. However, M2 macrophages and CD4+ T cells play essential roles during AVF maturation, suggesting that total immunosuppression may suppress adaptive vascular remodeling. Therefore, it is likely that regulation of inflammation during fistula maturation will require a balanced approach to coordinate the various inflammatory cell subsets. Advances in immunosuppressive drug development and delivery systems may allow for more targeted regulation of inflammation to improve vascular remodeling and enhance AVF maturation. (JVS–Vascular Science 2020;1:207-18.) : Clinical Relevance: Patients with end-stage renal failure depend on successful AVF maturation to have a useful access. Inflammation occurs during fistula maturation and may be a therapeutic target to improve fistula maturation and utilization. Inflammation is mainly caused by T cells and macrophages, which have several subsets with distinct phenotypes and roles during vascular remodeling. 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callnumber-first	R - Medicine
author	Yutaka Matsubara, MD, PhD
spellingShingle	Yutaka Matsubara, MD, PhD misc RC666-701 misc Arteriovenous fistula misc Inflammation misc T-cells misc Macrophages misc Vascular remodeling misc Diseases of the circulatory (Cardiovascular) system Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation
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topic_title	RC666-701 Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation Arteriovenous fistula Inflammation T-cells Macrophages Vascular remodeling
topic	misc RC666-701 misc Arteriovenous fistula misc Inflammation misc T-cells misc Macrophages misc Vascular remodeling misc Diseases of the circulatory (Cardiovascular) system
topic_unstemmed	misc RC666-701 misc Arteriovenous fistula misc Inflammation misc T-cells misc Macrophages misc Vascular remodeling misc Diseases of the circulatory (Cardiovascular) system
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title	Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation
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title_full	Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation
author_sort	Yutaka Matsubara, MD, PhD
journal	JVS - Vascular Science
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author_browse	Yutaka Matsubara, MD, PhD Gathe Kiwan, MS Arash Fereydooni, MD John Langford, MD Alan Dardik, MD, PhD
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title_sort	distinct subsets of t cells and macrophages impact venous remodeling during arteriovenous fistula maturation
callnumber	RC666-701
title_auth	Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation
abstract	Patients with end-stage renal failure depend on hemodialysis indefinitely without renal transplantation, requiring a long-term patent vascular access. Although an arteriovenous fistula (AVF) remains the preferred vascular access for hemodialysis because of its longer patency and fewer complications compared with other vascular accesses, the primary patency of AVF is only 50% to 60%, presenting a clinical need for improvement. AVF mature by developing a thickened vascular wall and increased diameter to adapt to arterial blood pressure and flow volume. Inflammation plays a critical role during vascular remodeling and fistula maturation; increased shear stress triggers infiltration of T cells and macrophages that initiate inflammation, with involvement of several different subsets of T cells and macrophages. We review the literature describing distinct roles of the various subsets of T cells and macrophages during vascular remodeling. Immunosuppression with sirolimus or prednisolone decreases neointimal hyperplasia during AVF maturation, suggesting novel approaches to enhance vascular remodeling. However, M2 macrophages and CD4+ T cells play essential roles during AVF maturation, suggesting that total immunosuppression may suppress adaptive vascular remodeling. Therefore, it is likely that regulation of inflammation during fistula maturation will require a balanced approach to coordinate the various inflammatory cell subsets. Advances in immunosuppressive drug development and delivery systems may allow for more targeted regulation of inflammation to improve vascular remodeling and enhance AVF maturation. (JVS–Vascular Science 2020;1:207-18.) : Clinical Relevance: Patients with end-stage renal failure depend on successful AVF maturation to have a useful access. Inflammation occurs during fistula maturation and may be a therapeutic target to improve fistula maturation and utilization. Inflammation is mainly caused by T cells and macrophages, which have several subsets with distinct phenotypes and roles during vascular remodeling. Regulation of inflammation during fistula maturation requires a balanced approach to coordinate the various inflammatory cell subsets.
abstractGer	Patients with end-stage renal failure depend on hemodialysis indefinitely without renal transplantation, requiring a long-term patent vascular access. Although an arteriovenous fistula (AVF) remains the preferred vascular access for hemodialysis because of its longer patency and fewer complications compared with other vascular accesses, the primary patency of AVF is only 50% to 60%, presenting a clinical need for improvement. AVF mature by developing a thickened vascular wall and increased diameter to adapt to arterial blood pressure and flow volume. Inflammation plays a critical role during vascular remodeling and fistula maturation; increased shear stress triggers infiltration of T cells and macrophages that initiate inflammation, with involvement of several different subsets of T cells and macrophages. We review the literature describing distinct roles of the various subsets of T cells and macrophages during vascular remodeling. Immunosuppression with sirolimus or prednisolone decreases neointimal hyperplasia during AVF maturation, suggesting novel approaches to enhance vascular remodeling. However, M2 macrophages and CD4+ T cells play essential roles during AVF maturation, suggesting that total immunosuppression may suppress adaptive vascular remodeling. Therefore, it is likely that regulation of inflammation during fistula maturation will require a balanced approach to coordinate the various inflammatory cell subsets. Advances in immunosuppressive drug development and delivery systems may allow for more targeted regulation of inflammation to improve vascular remodeling and enhance AVF maturation. (JVS–Vascular Science 2020;1:207-18.) : Clinical Relevance: Patients with end-stage renal failure depend on successful AVF maturation to have a useful access. Inflammation occurs during fistula maturation and may be a therapeutic target to improve fistula maturation and utilization. Inflammation is mainly caused by T cells and macrophages, which have several subsets with distinct phenotypes and roles during vascular remodeling. Regulation of inflammation during fistula maturation requires a balanced approach to coordinate the various inflammatory cell subsets.
abstract_unstemmed	Patients with end-stage renal failure depend on hemodialysis indefinitely without renal transplantation, requiring a long-term patent vascular access. Although an arteriovenous fistula (AVF) remains the preferred vascular access for hemodialysis because of its longer patency and fewer complications compared with other vascular accesses, the primary patency of AVF is only 50% to 60%, presenting a clinical need for improvement. AVF mature by developing a thickened vascular wall and increased diameter to adapt to arterial blood pressure and flow volume. Inflammation plays a critical role during vascular remodeling and fistula maturation; increased shear stress triggers infiltration of T cells and macrophages that initiate inflammation, with involvement of several different subsets of T cells and macrophages. We review the literature describing distinct roles of the various subsets of T cells and macrophages during vascular remodeling. Immunosuppression with sirolimus or prednisolone decreases neointimal hyperplasia during AVF maturation, suggesting novel approaches to enhance vascular remodeling. However, M2 macrophages and CD4+ T cells play essential roles during AVF maturation, suggesting that total immunosuppression may suppress adaptive vascular remodeling. Therefore, it is likely that regulation of inflammation during fistula maturation will require a balanced approach to coordinate the various inflammatory cell subsets. Advances in immunosuppressive drug development and delivery systems may allow for more targeted regulation of inflammation to improve vascular remodeling and enhance AVF maturation. (JVS–Vascular Science 2020;1:207-18.) : Clinical Relevance: Patients with end-stage renal failure depend on successful AVF maturation to have a useful access. Inflammation occurs during fistula maturation and may be a therapeutic target to improve fistula maturation and utilization. Inflammation is mainly caused by T cells and macrophages, which have several subsets with distinct phenotypes and roles during vascular remodeling. Regulation of inflammation during fistula maturation requires a balanced approach to coordinate the various inflammatory cell subsets.
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title_short	Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation
url	https://doi.org/10.1016/j.jvssci.2020.07.005 https://doaj.org/article/612afa44646f40e6a75ab2adb622ce40 http://www.sciencedirect.com/science/article/pii/S2666350320300171 https://doaj.org/toc/2666-3503
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up_date	2024-07-03T15:20:50.589Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ070539480</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230309093424.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230228s2020 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.jvssci.2020.07.005</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ070539480</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ612afa44646f40e6a75ab2adb622ce40</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="050" ind1=" " ind2="0"><subfield code="a">RC666-701</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Yutaka Matsubara, MD, PhD</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020</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">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Patients with end-stage renal failure depend on hemodialysis indefinitely without renal transplantation, requiring a long-term patent vascular access. Although an arteriovenous fistula (AVF) remains the preferred vascular access for hemodialysis because of its longer patency and fewer complications compared with other vascular accesses, the primary patency of AVF is only 50% to 60%, presenting a clinical need for improvement. AVF mature by developing a thickened vascular wall and increased diameter to adapt to arterial blood pressure and flow volume. Inflammation plays a critical role during vascular remodeling and fistula maturation; increased shear stress triggers infiltration of T cells and macrophages that initiate inflammation, with involvement of several different subsets of T cells and macrophages. We review the literature describing distinct roles of the various subsets of T cells and macrophages during vascular remodeling. Immunosuppression with sirolimus or prednisolone decreases neointimal hyperplasia during AVF maturation, suggesting novel approaches to enhance vascular remodeling. However, M2 macrophages and CD4+ T cells play essential roles during AVF maturation, suggesting that total immunosuppression may suppress adaptive vascular remodeling. Therefore, it is likely that regulation of inflammation during fistula maturation will require a balanced approach to coordinate the various inflammatory cell subsets. Advances in immunosuppressive drug development and delivery systems may allow for more targeted regulation of inflammation to improve vascular remodeling and enhance AVF maturation. (JVS–Vascular Science 2020;1:207-18.) : Clinical Relevance: Patients with end-stage renal failure depend on successful AVF maturation to have a useful access. Inflammation occurs during fistula maturation and may be a therapeutic target to improve fistula maturation and utilization. Inflammation is mainly caused by T cells and macrophages, which have several subsets with distinct phenotypes and roles during vascular remodeling. 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Distinct subsets of T cells and macrophages impact venous remodeling during arteriovenous fistula maturation

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