Mild Therapeutic Hypothermia Alleviated Myocardial Ischemia/Reperfusion Injury via Targeting SLC25A10 to Suppress Mitochondrial Apoptosis-Reference-Cited by-同舟云学术

Mild Therapeutic Hypothermia Alleviated Myocardial Ischemia/Reperfusion Injury via Targeting SLC25A10 to Suppress Mitochondrial Apoptosis

Published:2024-04-03 Issue:4 Volume:17 Page:946-958
ISSN:1937-5387
Container-title:Journal of Cardiovascular Translational Research
language:en
Short-container-title:J. of Cardiovasc. Trans. Res.

Author:

Ma Senlin,Song Yun,Xu Yanxin,Wang Chao,Yang Yifan,Zheng Yanchao,Lu Qiuxin,Chen Qingjiang,Wu Jian,Wang Bin^ORCID,Chen Mingquan

Abstract

AbstractMyocardial ischemia/reperfusion injury (MI/RI) is identified as a severe vascular emergency, and the treatment strategy of MI/RI still needs further improvement. The present study aimed to investigate the potential effects of mild therapeutic hypothermia (MTH) on MI/RI and underlying mechanisms. In ischemia/reperfusion (I/R) rats, MTH treatment significantly improved myocardial injury, attenuated myocardial infarction, and inhibited the mitochondrial apoptosis pathway. The results of proteomics identified SLC25A10 as the main target of MTH treatment. Consistently, SLC25A10 expressions in I/R rat myocardium and hypoxia and reoxygenation (H/R) cardiomyocytes were significantly suppressed, which was effectively reversed by MTH treatment. In H/R cardiomyocytes, MTH treatment significantly improved cell injury, mitochondrial dysfunction, and inhibited the mitochondrial apoptosis pathway, which were partially reversed by SLC25A10 deletion. These findings suggested that MTH treatment could protect against MI/RI by modulating SLC25A10 expression to suppress mitochondrial apoptosis pathway, providing new theoretical basis for clinical application of MTH treatment for MI/RI. Graphical Abstract

Funder

National Natural Science Foundation of China

Publisher

Springer Science and Business Media LLC

Link

https://link.springer.com/content/pdf/10.1007/s12265-024-10503-z.pdf

Reference33 articles.

1. Global Health Estimates 2016. Deaths by cause, age, sex, by country and by region, 2000–2016. Geneva, Switzerland: World Health Organization; 2018.

2. Lu L, Liu M, Sun R, Zheng Y, Zhang P. Myocardial infarction: symptoms and treatments. Cell Biochem Biophys. 2015;72(3):865–7. https://doi.org/10.1007/s12013-015-0553-4.

3. Hausenloy DJ, Yellon DM. Myocardial ischemia-reperfusion injury: a neglected therapeutic target. J Clin Invest. 2013;123(1):92–100. https://doi.org/10.1172/JCI62874.

4. Neubauer S. The failing heart—an engine out of fuel. N Engl J Med. 2007;356(11):1140–51. https://doi.org/10.1056/NEJMra063052.

5. Morciano G, Giorgi C, Bonora M, et al. Molecular identity of the mitochondrial permeability transition pore and its role in ischemia-reperfusion injury. J Mol Cell Cardiol. 2015;78:142–53. https://doi.org/10.1016/j.yjmcc.2014.08.015.