Cardiomyocytes Cellular Phenotypes After Myocardial Infarction

Despite the increasing success of interventional coronary reperfusion strategies, mortality related to acute myocardial infarction (MI) is still substantial. MI is defined as sudden death of myocardial tissue caused by an ischemic episode. Ischaemia leads to adverse remodelling in the affected myoca...

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Autores principales:	Alessandra Maria Lodrini, Marie-José Goumans
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	myocardial infarction apoptosis autophagy inflammation senescence dedifferentiation Diseases of the circulatory (Cardiovascular) system RC666-701
Acceso en línea:	https://doaj.org/article/4d3831eae5ed44b480ca2e9d3edf421a
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spelling	oai:doaj.org-article:4d3831eae5ed44b480ca2e9d3edf421a2021-11-08T07:03:46ZCardiomyocytes Cellular Phenotypes After Myocardial Infarction2297-055X10.3389/fcvm.2021.750510https://doaj.org/article/4d3831eae5ed44b480ca2e9d3edf421a2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fcvm.2021.750510/fullhttps://doaj.org/toc/2297-055XDespite the increasing success of interventional coronary reperfusion strategies, mortality related to acute myocardial infarction (MI) is still substantial. MI is defined as sudden death of myocardial tissue caused by an ischemic episode. Ischaemia leads to adverse remodelling in the affected myocardium, inducing metabolic and ionic perturbations at a single cell level, ultimately leading to cell death. The adult mammalian heart has limited regenerative capacity to replace lost cells. Identifying and enhancing physiological cardioprotective processes may be a promising therapy for patients with MI. Studies report an increasing amount of evidence stating the intricacy of the pathophysiology of the infarcted heart. Besides apoptosis, other cellular phenotypes have emerged as key players in the ischemic myocardium, in particular senescence, inflammation, and dedifferentiation. Furthermore, some cardiomyocytes in the infarct border zone uncouple from the surviving myocardium and dedifferentiate, while other cells become senescent in response to injury and start to produce a pro-inflammatory secretome. Enhancing electric coupling between cardiomyocytes in the border zone, eliminating senescent cells with senolytic compounds, and upregulating cardioprotective cellular processes like autophagy, may increase the number of functional cardiomyocytes and therefore enhance cardiac contractility. This review describes the different cellular phenotypes and pathways implicated in injury, remodelling, and regeneration of the myocardium after MI. Moreover, we discuss implications of the complex pathophysiological attributes of the infarcted heart in designing new therapeutic strategies.Alessandra Maria LodriniMarie-José GoumansFrontiers Media S.A.articlemyocardial infarctionapoptosisautophagyinflammationsenescencededifferentiationDiseases of the circulatory (Cardiovascular) systemRC666-701ENFrontiers in Cardiovascular Medicine, Vol 8 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	myocardial infarction apoptosis autophagy inflammation senescence dedifferentiation Diseases of the circulatory (Cardiovascular) system RC666-701
spellingShingle	myocardial infarction apoptosis autophagy inflammation senescence dedifferentiation Diseases of the circulatory (Cardiovascular) system RC666-701 Alessandra Maria Lodrini Marie-José Goumans Cardiomyocytes Cellular Phenotypes After Myocardial Infarction
description	Despite the increasing success of interventional coronary reperfusion strategies, mortality related to acute myocardial infarction (MI) is still substantial. MI is defined as sudden death of myocardial tissue caused by an ischemic episode. Ischaemia leads to adverse remodelling in the affected myocardium, inducing metabolic and ionic perturbations at a single cell level, ultimately leading to cell death. The adult mammalian heart has limited regenerative capacity to replace lost cells. Identifying and enhancing physiological cardioprotective processes may be a promising therapy for patients with MI. Studies report an increasing amount of evidence stating the intricacy of the pathophysiology of the infarcted heart. Besides apoptosis, other cellular phenotypes have emerged as key players in the ischemic myocardium, in particular senescence, inflammation, and dedifferentiation. Furthermore, some cardiomyocytes in the infarct border zone uncouple from the surviving myocardium and dedifferentiate, while other cells become senescent in response to injury and start to produce a pro-inflammatory secretome. Enhancing electric coupling between cardiomyocytes in the border zone, eliminating senescent cells with senolytic compounds, and upregulating cardioprotective cellular processes like autophagy, may increase the number of functional cardiomyocytes and therefore enhance cardiac contractility. This review describes the different cellular phenotypes and pathways implicated in injury, remodelling, and regeneration of the myocardium after MI. Moreover, we discuss implications of the complex pathophysiological attributes of the infarcted heart in designing new therapeutic strategies.
format	article
author	Alessandra Maria Lodrini Marie-José Goumans
author_facet	Alessandra Maria Lodrini Marie-José Goumans
author_sort	Alessandra Maria Lodrini
title	Cardiomyocytes Cellular Phenotypes After Myocardial Infarction
title_short	Cardiomyocytes Cellular Phenotypes After Myocardial Infarction
title_full	Cardiomyocytes Cellular Phenotypes After Myocardial Infarction
title_fullStr	Cardiomyocytes Cellular Phenotypes After Myocardial Infarction
title_full_unstemmed	Cardiomyocytes Cellular Phenotypes After Myocardial Infarction
title_sort	cardiomyocytes cellular phenotypes after myocardial infarction
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/4d3831eae5ed44b480ca2e9d3edf421a
work_keys_str_mv	AT alessandramarialodrini cardiomyocytescellularphenotypesaftermyocardialinfarction AT mariejosegoumans cardiomyocytescellularphenotypesaftermyocardialinfarction
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Cardiomyocytes Cellular Phenotypes After Myocardial Infarction

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