The Mechanobiology of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease

Endothelial cells (ECs) lining the cardiovascular system are subjected to a highly dynamic microenvironment resulting from pulsatile pressure and circulating blood flow. Endothelial cells are remarkably sensitive to these forces, which are transduced to activate signaling pathways to maintain endoth...
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Autor*in:	Shahrin Islam [verfasserIn] Kristina I. Boström [verfasserIn] Dino Di Carlo [verfasserIn] Craig A. Simmons [verfasserIn] Yin Tintut [verfasserIn] Yucheng Yao [verfasserIn] Jeffrey J. Hsu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	endothelial-to-mesenchymal transition mechanobiology cardiovascular disease endothelial mesenchymal biomechanical

Übergeordnetes Werk:	In: Frontiers in Physiology - Frontiers Media S.A., 2011, 12(2021)
Übergeordnetes Werk:	volume:12 ; year:2021

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fphys.2021.734215

Katalog-ID:	DOAJ061968382

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520			\|a Endothelial cells (ECs) lining the cardiovascular system are subjected to a highly dynamic microenvironment resulting from pulsatile pressure and circulating blood flow. Endothelial cells are remarkably sensitive to these forces, which are transduced to activate signaling pathways to maintain endothelial homeostasis and respond to changes in the environment. Aberrations in these biomechanical stresses, however, can trigger changes in endothelial cell phenotype and function. One process involved in this cellular plasticity is endothelial-to-mesenchymal transition (EndMT). As a result of EndMT, ECs lose cell-cell adhesion, alter their cytoskeletal organization, and gain increased migratory and invasive capabilities. EndMT has long been known to occur during cardiovascular development, but there is now a growing body of evidence also implicating it in many cardiovascular diseases (CVD), often associated with alterations in the cellular mechanical environment. In this review, we highlight the emerging role of shear stress, cyclic strain, matrix stiffness, and composition associated with EndMT in CVD. We first provide an overview of EndMT and context for how ECs sense, transduce, and respond to certain mechanical stimuli. We then describe the biomechanical features of EndMT and the role of mechanically driven EndMT in CVD. Finally, we indicate areas of open investigation to further elucidate the complexity of EndMT in the cardiovascular system. Understanding the mechanistic underpinnings of the mechanobiology of EndMT in CVD can provide insight into new opportunities for identification of novel diagnostic markers and therapeutic interventions.
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allfields	10.3389/fphys.2021.734215 doi (DE-627)DOAJ061968382 (DE-599)DOAJ40f73fe5098f4e64b8292f2ec747c7bc DE-627 ger DE-627 rakwb eng QP1-981 Shahrin Islam verfasserin aut The Mechanobiology of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Endothelial cells (ECs) lining the cardiovascular system are subjected to a highly dynamic microenvironment resulting from pulsatile pressure and circulating blood flow. Endothelial cells are remarkably sensitive to these forces, which are transduced to activate signaling pathways to maintain endothelial homeostasis and respond to changes in the environment. Aberrations in these biomechanical stresses, however, can trigger changes in endothelial cell phenotype and function. One process involved in this cellular plasticity is endothelial-to-mesenchymal transition (EndMT). As a result of EndMT, ECs lose cell-cell adhesion, alter their cytoskeletal organization, and gain increased migratory and invasive capabilities. EndMT has long been known to occur during cardiovascular development, but there is now a growing body of evidence also implicating it in many cardiovascular diseases (CVD), often associated with alterations in the cellular mechanical environment. In this review, we highlight the emerging role of shear stress, cyclic strain, matrix stiffness, and composition associated with EndMT in CVD. We first provide an overview of EndMT and context for how ECs sense, transduce, and respond to certain mechanical stimuli. We then describe the biomechanical features of EndMT and the role of mechanically driven EndMT in CVD. Finally, we indicate areas of open investigation to further elucidate the complexity of EndMT in the cardiovascular system. Understanding the mechanistic underpinnings of the mechanobiology of EndMT in CVD can provide insight into new opportunities for identification of novel diagnostic markers and therapeutic interventions. endothelial-to-mesenchymal transition mechanobiology cardiovascular disease endothelial mesenchymal biomechanical Physiology Kristina I. Boström verfasserin aut Kristina I. Boström verfasserin aut Kristina I. Boström verfasserin aut Dino Di Carlo verfasserin aut Dino Di Carlo verfasserin aut Craig A. Simmons verfasserin aut Craig A. Simmons verfasserin aut Craig A. Simmons verfasserin aut Yin Tintut verfasserin aut Yin Tintut verfasserin aut Yin Tintut verfasserin aut Yucheng Yao verfasserin aut Jeffrey J. Hsu verfasserin aut Jeffrey J. Hsu verfasserin aut In Frontiers in Physiology Frontiers Media S.A., 2011 12(2021) (DE-627)631498788 (DE-600)2564217-0 1664042X nnns volume:12 year:2021 https://doi.org/10.3389/fphys.2021.734215 kostenfrei https://doaj.org/article/40f73fe5098f4e64b8292f2ec747c7bc kostenfrei https://www.frontiersin.org/articles/10.3389/fphys.2021.734215/full kostenfrei https://doaj.org/toc/1664-042X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021
spelling	10.3389/fphys.2021.734215 doi (DE-627)DOAJ061968382 (DE-599)DOAJ40f73fe5098f4e64b8292f2ec747c7bc DE-627 ger DE-627 rakwb eng QP1-981 Shahrin Islam verfasserin aut The Mechanobiology of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Endothelial cells (ECs) lining the cardiovascular system are subjected to a highly dynamic microenvironment resulting from pulsatile pressure and circulating blood flow. Endothelial cells are remarkably sensitive to these forces, which are transduced to activate signaling pathways to maintain endothelial homeostasis and respond to changes in the environment. Aberrations in these biomechanical stresses, however, can trigger changes in endothelial cell phenotype and function. One process involved in this cellular plasticity is endothelial-to-mesenchymal transition (EndMT). As a result of EndMT, ECs lose cell-cell adhesion, alter their cytoskeletal organization, and gain increased migratory and invasive capabilities. EndMT has long been known to occur during cardiovascular development, but there is now a growing body of evidence also implicating it in many cardiovascular diseases (CVD), often associated with alterations in the cellular mechanical environment. In this review, we highlight the emerging role of shear stress, cyclic strain, matrix stiffness, and composition associated with EndMT in CVD. We first provide an overview of EndMT and context for how ECs sense, transduce, and respond to certain mechanical stimuli. We then describe the biomechanical features of EndMT and the role of mechanically driven EndMT in CVD. Finally, we indicate areas of open investigation to further elucidate the complexity of EndMT in the cardiovascular system. Understanding the mechanistic underpinnings of the mechanobiology of EndMT in CVD can provide insight into new opportunities for identification of novel diagnostic markers and therapeutic interventions. endothelial-to-mesenchymal transition mechanobiology cardiovascular disease endothelial mesenchymal biomechanical Physiology Kristina I. Boström verfasserin aut Kristina I. Boström verfasserin aut Kristina I. Boström verfasserin aut Dino Di Carlo verfasserin aut Dino Di Carlo verfasserin aut Craig A. Simmons verfasserin aut Craig A. Simmons verfasserin aut Craig A. Simmons verfasserin aut Yin Tintut verfasserin aut Yin Tintut verfasserin aut Yin Tintut verfasserin aut Yucheng Yao verfasserin aut Jeffrey J. Hsu verfasserin aut Jeffrey J. Hsu verfasserin aut In Frontiers in Physiology Frontiers Media S.A., 2011 12(2021) (DE-627)631498788 (DE-600)2564217-0 1664042X nnns volume:12 year:2021 https://doi.org/10.3389/fphys.2021.734215 kostenfrei https://doaj.org/article/40f73fe5098f4e64b8292f2ec747c7bc kostenfrei https://www.frontiersin.org/articles/10.3389/fphys.2021.734215/full kostenfrei https://doaj.org/toc/1664-042X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021
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allfieldsGer	10.3389/fphys.2021.734215 doi (DE-627)DOAJ061968382 (DE-599)DOAJ40f73fe5098f4e64b8292f2ec747c7bc DE-627 ger DE-627 rakwb eng QP1-981 Shahrin Islam verfasserin aut The Mechanobiology of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Endothelial cells (ECs) lining the cardiovascular system are subjected to a highly dynamic microenvironment resulting from pulsatile pressure and circulating blood flow. Endothelial cells are remarkably sensitive to these forces, which are transduced to activate signaling pathways to maintain endothelial homeostasis and respond to changes in the environment. Aberrations in these biomechanical stresses, however, can trigger changes in endothelial cell phenotype and function. One process involved in this cellular plasticity is endothelial-to-mesenchymal transition (EndMT). As a result of EndMT, ECs lose cell-cell adhesion, alter their cytoskeletal organization, and gain increased migratory and invasive capabilities. EndMT has long been known to occur during cardiovascular development, but there is now a growing body of evidence also implicating it in many cardiovascular diseases (CVD), often associated with alterations in the cellular mechanical environment. In this review, we highlight the emerging role of shear stress, cyclic strain, matrix stiffness, and composition associated with EndMT in CVD. We first provide an overview of EndMT and context for how ECs sense, transduce, and respond to certain mechanical stimuli. We then describe the biomechanical features of EndMT and the role of mechanically driven EndMT in CVD. Finally, we indicate areas of open investigation to further elucidate the complexity of EndMT in the cardiovascular system. Understanding the mechanistic underpinnings of the mechanobiology of EndMT in CVD can provide insight into new opportunities for identification of novel diagnostic markers and therapeutic interventions. endothelial-to-mesenchymal transition mechanobiology cardiovascular disease endothelial mesenchymal biomechanical Physiology Kristina I. Boström verfasserin aut Kristina I. Boström verfasserin aut Kristina I. Boström verfasserin aut Dino Di Carlo verfasserin aut Dino Di Carlo verfasserin aut Craig A. Simmons verfasserin aut Craig A. Simmons verfasserin aut Craig A. Simmons verfasserin aut Yin Tintut verfasserin aut Yin Tintut verfasserin aut Yin Tintut verfasserin aut Yucheng Yao verfasserin aut Jeffrey J. Hsu verfasserin aut Jeffrey J. Hsu verfasserin aut In Frontiers in Physiology Frontiers Media S.A., 2011 12(2021) (DE-627)631498788 (DE-600)2564217-0 1664042X nnns volume:12 year:2021 https://doi.org/10.3389/fphys.2021.734215 kostenfrei https://doaj.org/article/40f73fe5098f4e64b8292f2ec747c7bc kostenfrei https://www.frontiersin.org/articles/10.3389/fphys.2021.734215/full kostenfrei https://doaj.org/toc/1664-042X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021
allfieldsSound	10.3389/fphys.2021.734215 doi (DE-627)DOAJ061968382 (DE-599)DOAJ40f73fe5098f4e64b8292f2ec747c7bc DE-627 ger DE-627 rakwb eng QP1-981 Shahrin Islam verfasserin aut The Mechanobiology of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Endothelial cells (ECs) lining the cardiovascular system are subjected to a highly dynamic microenvironment resulting from pulsatile pressure and circulating blood flow. Endothelial cells are remarkably sensitive to these forces, which are transduced to activate signaling pathways to maintain endothelial homeostasis and respond to changes in the environment. Aberrations in these biomechanical stresses, however, can trigger changes in endothelial cell phenotype and function. One process involved in this cellular plasticity is endothelial-to-mesenchymal transition (EndMT). As a result of EndMT, ECs lose cell-cell adhesion, alter their cytoskeletal organization, and gain increased migratory and invasive capabilities. EndMT has long been known to occur during cardiovascular development, but there is now a growing body of evidence also implicating it in many cardiovascular diseases (CVD), often associated with alterations in the cellular mechanical environment. In this review, we highlight the emerging role of shear stress, cyclic strain, matrix stiffness, and composition associated with EndMT in CVD. We first provide an overview of EndMT and context for how ECs sense, transduce, and respond to certain mechanical stimuli. We then describe the biomechanical features of EndMT and the role of mechanically driven EndMT in CVD. Finally, we indicate areas of open investigation to further elucidate the complexity of EndMT in the cardiovascular system. Understanding the mechanistic underpinnings of the mechanobiology of EndMT in CVD can provide insight into new opportunities for identification of novel diagnostic markers and therapeutic interventions. endothelial-to-mesenchymal transition mechanobiology cardiovascular disease endothelial mesenchymal biomechanical Physiology Kristina I. Boström verfasserin aut Kristina I. Boström verfasserin aut Kristina I. Boström verfasserin aut Dino Di Carlo verfasserin aut Dino Di Carlo verfasserin aut Craig A. Simmons verfasserin aut Craig A. Simmons verfasserin aut Craig A. Simmons verfasserin aut Yin Tintut verfasserin aut Yin Tintut verfasserin aut Yin Tintut verfasserin aut Yucheng Yao verfasserin aut Jeffrey J. Hsu verfasserin aut Jeffrey J. Hsu verfasserin aut In Frontiers in Physiology Frontiers Media S.A., 2011 12(2021) (DE-627)631498788 (DE-600)2564217-0 1664042X nnns volume:12 year:2021 https://doi.org/10.3389/fphys.2021.734215 kostenfrei https://doaj.org/article/40f73fe5098f4e64b8292f2ec747c7bc kostenfrei https://www.frontiersin.org/articles/10.3389/fphys.2021.734215/full kostenfrei https://doaj.org/toc/1664-042X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021
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author	Shahrin Islam
spellingShingle	Shahrin Islam misc QP1-981 misc endothelial-to-mesenchymal transition misc mechanobiology misc cardiovascular disease misc endothelial misc mesenchymal misc biomechanical misc Physiology The Mechanobiology of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease
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title_sort	mechanobiology of endothelial-to-mesenchymal transition in cardiovascular disease
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title_auth	The Mechanobiology of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease
abstract	Endothelial cells (ECs) lining the cardiovascular system are subjected to a highly dynamic microenvironment resulting from pulsatile pressure and circulating blood flow. Endothelial cells are remarkably sensitive to these forces, which are transduced to activate signaling pathways to maintain endothelial homeostasis and respond to changes in the environment. Aberrations in these biomechanical stresses, however, can trigger changes in endothelial cell phenotype and function. One process involved in this cellular plasticity is endothelial-to-mesenchymal transition (EndMT). As a result of EndMT, ECs lose cell-cell adhesion, alter their cytoskeletal organization, and gain increased migratory and invasive capabilities. EndMT has long been known to occur during cardiovascular development, but there is now a growing body of evidence also implicating it in many cardiovascular diseases (CVD), often associated with alterations in the cellular mechanical environment. In this review, we highlight the emerging role of shear stress, cyclic strain, matrix stiffness, and composition associated with EndMT in CVD. We first provide an overview of EndMT and context for how ECs sense, transduce, and respond to certain mechanical stimuli. We then describe the biomechanical features of EndMT and the role of mechanically driven EndMT in CVD. Finally, we indicate areas of open investigation to further elucidate the complexity of EndMT in the cardiovascular system. Understanding the mechanistic underpinnings of the mechanobiology of EndMT in CVD can provide insight into new opportunities for identification of novel diagnostic markers and therapeutic interventions.
abstractGer	Endothelial cells (ECs) lining the cardiovascular system are subjected to a highly dynamic microenvironment resulting from pulsatile pressure and circulating blood flow. Endothelial cells are remarkably sensitive to these forces, which are transduced to activate signaling pathways to maintain endothelial homeostasis and respond to changes in the environment. Aberrations in these biomechanical stresses, however, can trigger changes in endothelial cell phenotype and function. One process involved in this cellular plasticity is endothelial-to-mesenchymal transition (EndMT). As a result of EndMT, ECs lose cell-cell adhesion, alter their cytoskeletal organization, and gain increased migratory and invasive capabilities. EndMT has long been known to occur during cardiovascular development, but there is now a growing body of evidence also implicating it in many cardiovascular diseases (CVD), often associated with alterations in the cellular mechanical environment. In this review, we highlight the emerging role of shear stress, cyclic strain, matrix stiffness, and composition associated with EndMT in CVD. We first provide an overview of EndMT and context for how ECs sense, transduce, and respond to certain mechanical stimuli. We then describe the biomechanical features of EndMT and the role of mechanically driven EndMT in CVD. Finally, we indicate areas of open investigation to further elucidate the complexity of EndMT in the cardiovascular system. Understanding the mechanistic underpinnings of the mechanobiology of EndMT in CVD can provide insight into new opportunities for identification of novel diagnostic markers and therapeutic interventions.
abstract_unstemmed	Endothelial cells (ECs) lining the cardiovascular system are subjected to a highly dynamic microenvironment resulting from pulsatile pressure and circulating blood flow. Endothelial cells are remarkably sensitive to these forces, which are transduced to activate signaling pathways to maintain endothelial homeostasis and respond to changes in the environment. Aberrations in these biomechanical stresses, however, can trigger changes in endothelial cell phenotype and function. One process involved in this cellular plasticity is endothelial-to-mesenchymal transition (EndMT). As a result of EndMT, ECs lose cell-cell adhesion, alter their cytoskeletal organization, and gain increased migratory and invasive capabilities. EndMT has long been known to occur during cardiovascular development, but there is now a growing body of evidence also implicating it in many cardiovascular diseases (CVD), often associated with alterations in the cellular mechanical environment. In this review, we highlight the emerging role of shear stress, cyclic strain, matrix stiffness, and composition associated with EndMT in CVD. We first provide an overview of EndMT and context for how ECs sense, transduce, and respond to certain mechanical stimuli. We then describe the biomechanical features of EndMT and the role of mechanically driven EndMT in CVD. Finally, we indicate areas of open investigation to further elucidate the complexity of EndMT in the cardiovascular system. Understanding the mechanistic underpinnings of the mechanobiology of EndMT in CVD can provide insight into new opportunities for identification of novel diagnostic markers and therapeutic interventions.
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title_short	The Mechanobiology of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease
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Endothelial cells are remarkably sensitive to these forces, which are transduced to activate signaling pathways to maintain endothelial homeostasis and respond to changes in the environment. Aberrations in these biomechanical stresses, however, can trigger changes in endothelial cell phenotype and function. One process involved in this cellular plasticity is endothelial-to-mesenchymal transition (EndMT). As a result of EndMT, ECs lose cell-cell adhesion, alter their cytoskeletal organization, and gain increased migratory and invasive capabilities. EndMT has long been known to occur during cardiovascular development, but there is now a growing body of evidence also implicating it in many cardiovascular diseases (CVD), often associated with alterations in the cellular mechanical environment. In this review, we highlight the emerging role of shear stress, cyclic strain, matrix stiffness, and composition associated with EndMT in CVD. We first provide an overview of EndMT and context for how ECs sense, transduce, and respond to certain mechanical stimuli. We then describe the biomechanical features of EndMT and the role of mechanically driven EndMT in CVD. Finally, we indicate areas of open investigation to further elucidate the complexity of EndMT in the cardiovascular system. 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The Mechanobiology of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease

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