» Articles » PMID: 35600331

Programmed Cell Death of Endothelial Cells in Myocardial Infarction and Its Potential Therapeutic Strategy

Overview
Publisher Wiley
Date 2022 May 23
PMID 35600331
Authors
Affiliations
Soon will be listed here.
Abstract

Cardiovascular disease, especially coronary artery disease and stroke, kills around one-third of the world's population, and myocardial infarction, a primary symptom of coronary heart disease, is a major worldwide health problem. Cardiovascular disease research has historically focused on promoting angiogenesis following myocardial damage. Myocardial vascular repair is crucial for improving myocardial infarction prognosis. Endothelial cells, the largest population of nonmyocytes within myocardial tissue, play an important role in angiogenesis. In recent years, different types of programmed cell death such as apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy have been described and found to be linked with cardiovascular diseases such as myocardial infarction, heart failure, and myocarditis. This will have important implications for reforming the treatment strategy of cardiovascular diseases. Different types of cell death of endothelial cells in myocardial infarction have been proposed, the roles and mechanisms of endothelial cell death in myocardial infarction are summarized in this review, and endothelial cell death inhibition as a therapeutic technique for treating myocardial infarction might be advantageous to human health.

Citing Articles

Modulating mitochondrial dynamics ameliorates left ventricular dysfunction by suppressing diverse cell death pathways after diabetic cardiomyopathy.

Zhi F, Pu X, Wei W, Liu L, Liu C, Chen Y Int J Med Sci. 2024; 21(12):2324-2333.

PMID: 39310254 PMC: 11413890. DOI: 10.7150/ijms.98065.


ZC3H13-Mediated m6A Modification Ameliorates Acute Myocardial Infarction through Preventing Inflammation, Oxidative Stress and Ferroptosis by Targeting lncRNA93358.

Cai J, Wang X, Wang Z, Sheng S, Tang F, Zhang Z Inflammation. 2024; .

PMID: 39107569 DOI: 10.1007/s10753-024-02116-0.


Roxadustat Attenuates Adverse Remodeling Following Myocardial Infarction in Mice.

Zaruba M, Staggl S, Ghadge S, Maurer T, Gavranovic-Novakovic J, Jeyakumar V Cells. 2024; 13(13.

PMID: 38994928 PMC: 11240812. DOI: 10.3390/cells13131074.


Single-cell RNA sequencing reveals hub genes of myocardial infarction-associated endothelial cells.

Wang H, Dou L BMC Cardiovasc Disord. 2024; 24(1):70.

PMID: 38267885 PMC: 10809747. DOI: 10.1186/s12872-024-03727-z.


Application of machine learning algorithms to construct and validate a prediction model for coronary heart disease risk in patients with periodontitis: a population-based study.

Wang Y, Ni B, Xiao Y, Lin Y, Jiang Y, Zhang Y Front Cardiovasc Med. 2023; 10:1296405.

PMID: 38094122 PMC: 10716467. DOI: 10.3389/fcvm.2023.1296405.

References
1.
Dikic I, Elazar Z . Mechanism and medical implications of mammalian autophagy. Nat Rev Mol Cell Biol. 2018; 19(6):349-364. DOI: 10.1038/s41580-018-0003-4. View

2.
Taabazuing C, Okondo M, Bachovchin D . Pyroptosis and Apoptosis Pathways Engage in Bidirectional Crosstalk in Monocytes and Macrophages. Cell Chem Biol. 2017; 24(4):507-514.e4. PMC: 5467448. DOI: 10.1016/j.chembiol.2017.03.009. View

3.
Liao Z, Chen Y, Duan C, Zhu K, Huang R, Zhao H . Cardiac telocytes inhibit cardiac microvascular endothelial cell apoptosis through exosomal miRNA-21-5p-targeted silencing to improve angiogenesis following myocardial infarction. Theranostics. 2021; 11(1):268-291. PMC: 7681094. DOI: 10.7150/thno.47021. View

4.
Chen Y, Li S, Zhang Y, Wang M, Li X, Liu S . The lncRNA Malat1 regulates microvascular function after myocardial infarction in mice via miR-26b-5p/Mfn1 axis-mediated mitochondrial dynamics. Redox Biol. 2021; 41:101910. PMC: 7937833. DOI: 10.1016/j.redox.2021.101910. View

5.
Wu X, Li Y, Zhang S, Zhou X . Ferroptosis as a novel therapeutic target for cardiovascular disease. Theranostics. 2021; 11(7):3052-3059. PMC: 7847684. DOI: 10.7150/thno.54113. View