Cargando…

Cell Death and Exosomes Regulation After Myocardial Infarction and Ischemia-Reperfusion

Cardiovascular disease (CVD) is the leading cause of death in the global population, accounting for about one-third of all deaths each year. Notably, with CVDs, myocardial damages result from myocardial infarction (MI) or cardiac arrhythmias caused by interrupted blood flow. Significantly, in the pr...

Descripción completa

Detalles Bibliográficos
Autores principales: Wu, Xun, Iroegbu, Chukwuemeka Daniel, Peng, Jun, Guo, Jianjun, Yang, Jinfu, Fan, Chengming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8220218/
https://www.ncbi.nlm.nih.gov/pubmed/34179002
http://dx.doi.org/10.3389/fcell.2021.673677
_version_ 1783711102168727552
author Wu, Xun
Iroegbu, Chukwuemeka Daniel
Peng, Jun
Guo, Jianjun
Yang, Jinfu
Fan, Chengming
author_facet Wu, Xun
Iroegbu, Chukwuemeka Daniel
Peng, Jun
Guo, Jianjun
Yang, Jinfu
Fan, Chengming
author_sort Wu, Xun
collection PubMed
description Cardiovascular disease (CVD) is the leading cause of death in the global population, accounting for about one-third of all deaths each year. Notably, with CVDs, myocardial damages result from myocardial infarction (MI) or cardiac arrhythmias caused by interrupted blood flow. Significantly, in the process of MI or myocardial ischemic-reperfusion (I/R) injury, both regulated and non-regulated cell death methods are involved. The critical factor for patients’ prognosis is the infarct area’s size, which determines the myocardial cells’ survival. Cell therapy for MI has been a research hotspot in recent years; however, exosomes secreted by cells have attracted much attention following shortcomings concerning immunogens. Exosomes are extracellular vesicles containing several biologically active substances such as lipids, nucleic acids, and proteins. New evidence suggests that exosomes play a crucial role in regulating cell death after MI as exosomes of various stem cells can participate in the cell damage process after MI. Hence, in the review herein, we focused on introducing various cell-derived exosomes to reduce cell death after MI by regulating the cell death pathway to understand myocardial repair mechanisms better and provide a reference for clinical treatment.
format Online
Article
Text
id pubmed-8220218
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-82202182021-06-24 Cell Death and Exosomes Regulation After Myocardial Infarction and Ischemia-Reperfusion Wu, Xun Iroegbu, Chukwuemeka Daniel Peng, Jun Guo, Jianjun Yang, Jinfu Fan, Chengming Front Cell Dev Biol Cell and Developmental Biology Cardiovascular disease (CVD) is the leading cause of death in the global population, accounting for about one-third of all deaths each year. Notably, with CVDs, myocardial damages result from myocardial infarction (MI) or cardiac arrhythmias caused by interrupted blood flow. Significantly, in the process of MI or myocardial ischemic-reperfusion (I/R) injury, both regulated and non-regulated cell death methods are involved. The critical factor for patients’ prognosis is the infarct area’s size, which determines the myocardial cells’ survival. Cell therapy for MI has been a research hotspot in recent years; however, exosomes secreted by cells have attracted much attention following shortcomings concerning immunogens. Exosomes are extracellular vesicles containing several biologically active substances such as lipids, nucleic acids, and proteins. New evidence suggests that exosomes play a crucial role in regulating cell death after MI as exosomes of various stem cells can participate in the cell damage process after MI. Hence, in the review herein, we focused on introducing various cell-derived exosomes to reduce cell death after MI by regulating the cell death pathway to understand myocardial repair mechanisms better and provide a reference for clinical treatment. Frontiers Media S.A. 2021-06-09 /pmc/articles/PMC8220218/ /pubmed/34179002 http://dx.doi.org/10.3389/fcell.2021.673677 Text en Copyright © 2021 Wu, Iroegbu, Peng, Guo, Yang and Fan. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cell and Developmental Biology
Wu, Xun
Iroegbu, Chukwuemeka Daniel
Peng, Jun
Guo, Jianjun
Yang, Jinfu
Fan, Chengming
Cell Death and Exosomes Regulation After Myocardial Infarction and Ischemia-Reperfusion
title Cell Death and Exosomes Regulation After Myocardial Infarction and Ischemia-Reperfusion
title_full Cell Death and Exosomes Regulation After Myocardial Infarction and Ischemia-Reperfusion
title_fullStr Cell Death and Exosomes Regulation After Myocardial Infarction and Ischemia-Reperfusion
title_full_unstemmed Cell Death and Exosomes Regulation After Myocardial Infarction and Ischemia-Reperfusion
title_short Cell Death and Exosomes Regulation After Myocardial Infarction and Ischemia-Reperfusion
title_sort cell death and exosomes regulation after myocardial infarction and ischemia-reperfusion
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8220218/
https://www.ncbi.nlm.nih.gov/pubmed/34179002
http://dx.doi.org/10.3389/fcell.2021.673677
work_keys_str_mv AT wuxun celldeathandexosomesregulationaftermyocardialinfarctionandischemiareperfusion
AT iroegbuchukwuemekadaniel celldeathandexosomesregulationaftermyocardialinfarctionandischemiareperfusion
AT pengjun celldeathandexosomesregulationaftermyocardialinfarctionandischemiareperfusion
AT guojianjun celldeathandexosomesregulationaftermyocardialinfarctionandischemiareperfusion
AT yangjinfu celldeathandexosomesregulationaftermyocardialinfarctionandischemiareperfusion
AT fanchengming celldeathandexosomesregulationaftermyocardialinfarctionandischemiareperfusion