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本文引用的文献

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Different signalling in infarcted and non-infarcted areas of rat failing hearts: A role of necroptosis and inflammation.大鼠衰竭心脏梗死区和非梗死区的不同信号转导:坏死性凋亡和炎症的作用。
J Cell Mol Med. 2019 Sep;23(9):6429-6441. doi: 10.1111/jcmm.14536. Epub 2019 Jul 21.
2
Ferroptotic cell death and TLR4/Trif signaling initiate neutrophil recruitment after heart transplantation.铁死亡细胞死亡和 TLR4/Trif 信号在心脏移植后引发中性粒细胞募集。
J Clin Invest. 2019 Feb 26;129(6):2293-2304. doi: 10.1172/JCI126428.
3
Ferroptosis as a target for protection against cardiomyopathy.铁死亡作为防治心肌病的靶点。
Proc Natl Acad Sci U S A. 2019 Feb 12;116(7):2672-2680. doi: 10.1073/pnas.1821022116. Epub 2019 Jan 28.
4
Inhibition of Phosphoglycerate Mutase 5 Reduces Necroptosis in Rat Hearts Following Ischemia/Reperfusion Through Suppression of Dynamin-Related Protein 1.磷酸甘油酸变位酶 5 的抑制通过抑制动力相关蛋白 1 减少大鼠心脏缺血/再灌注后的坏死性凋亡。
Cardiovasc Drugs Ther. 2019 Feb;33(1):13-23. doi: 10.1007/s10557-018-06848-8.
5
Cyclophilin D, Somehow a Master Regulator of Mitochondrial Function.亲环素 D,某种程度上是线粒体功能的主要调节因子。
Biomolecules. 2018 Dec 14;8(4):176. doi: 10.3390/biom8040176.
6
Mitochondrial Permeability Transition: A Molecular Lesion with Multiple Drug Targets.线粒体通透性转换:具有多种药物靶点的分子病变。
Trends Pharmacol Sci. 2019 Jan;40(1):50-70. doi: 10.1016/j.tips.2018.11.004. Epub 2018 Dec 6.
7
Pyroptosis versus necroptosis: similarities, differences, and crosstalk.细胞焦亡与细胞坏死:相似性、差异性和相互作用。
Cell Death Differ. 2019 Jan;26(1):99-114. doi: 10.1038/s41418-018-0212-6. Epub 2018 Oct 19.
8
Nuclear RIPK3 and MLKL contribute to cytosolic necrosome formation and necroptosis.细胞核中的RIPK3和MLKL有助于胞质坏死小体的形成和坏死性凋亡。
Commun Biol. 2018 Jan 22;1:6. doi: 10.1038/s42003-017-0007-1. eCollection 2018.
9
HS-1371, a novel kinase inhibitor of RIP3-mediated necroptosis.HS-1371,一种新型 RIP3 介导的坏死性凋亡激酶抑制剂。
Exp Mol Med. 2018 Sep 20;50(9):1-15. doi: 10.1038/s12276-018-0152-8.
10
The role of RIP3 in cardiomyocyte necrosis induced by mitochondrial damage of myocardial ischemia-reperfusion.RIP3 在心肌缺血再灌注损伤中线粒体损伤诱导的心肌细胞坏死中的作用。
Acta Biochim Biophys Sin (Shanghai). 2018 Nov 1;50(11):1131-1140. doi: 10.1093/abbs/gmy108.

评估心肌细胞死亡的指南。

Guidelines for evaluating myocardial cell death.

机构信息

Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska.

Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University of Bratislava, Bratislava, Slovakia.

出版信息

Am J Physiol Heart Circ Physiol. 2019 Nov 1;317(5):H891-H922. doi: 10.1152/ajpheart.00259.2019. Epub 2019 Aug 16.

DOI:10.1152/ajpheart.00259.2019
PMID:31418596
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6879915/
Abstract

Cell death is a fundamental process in cardiac pathologies. Recent studies have revealed multiple forms of cell death, and several of them have been demonstrated to underlie adverse cardiac remodeling and heart failure. With the expansion in the area of myocardial cell death and increasing concerns over rigor and reproducibility, it is important and timely to set a guideline for the best practices of evaluating myocardial cell death. There are six major forms of regulated cell death observed in cardiac pathologies, namely apoptosis, necroptosis, mitochondrial-mediated necrosis, pyroptosis, ferroptosis, and autophagic cell death. In this article, we describe the best methods to identify, measure, and evaluate these modes of myocardial cell death. In addition, we discuss the limitations of currently practiced myocardial cell death mechanisms.

摘要

细胞死亡是心脏病理学中的一个基本过程。最近的研究揭示了多种形式的细胞死亡,其中一些已被证明是导致心脏不良重构和心力衰竭的原因。随着心肌细胞死亡领域的不断扩展,以及对严谨性和可重复性的日益关注,制定评估心肌细胞死亡的最佳实践指南非常重要且及时。在心脏病理学中观察到六种主要的调节性细胞死亡形式,即细胞凋亡、坏死性凋亡、线粒体介导的坏死、细胞焦亡、铁死亡和自噬性细胞死亡。在本文中,我们描述了识别、测量和评估这些心肌细胞死亡方式的最佳方法。此外,我们还讨论了目前实践中细胞死亡机制的局限性。