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Mitophagy Regulators as Novel Targets in Sepsis-Induced Myocardial Dysfunction.

作者信息

Friedrich Katharina, Kappert Kai

机构信息

Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institute of Diagnostic Laboratory Medicine, Clinical Chemistry and Pathobiochemistry, Augustenburger Platz 1, 13353 Berlin, Germany; Leibniz Institute for Neurobiology, Brenneckestr. 6, 39118 Magdeburg, Germany.

Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institute of Diagnostic Laboratory Medicine, Clinical Chemistry and Pathobiochemistry, Augustenburger Platz 1, 13353 Berlin, Germany.

出版信息

JACC Basic Transl Sci. 2025 Aug;10(8):101290. doi: 10.1016/j.jacbts.2025.04.004.

DOI:10.1016/j.jacbts.2025.04.004
PMID:40866038
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12399166/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67de/12399166/c165b8e8554a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67de/12399166/454dd96c2c8f/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67de/12399166/c165b8e8554a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67de/12399166/454dd96c2c8f/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/67de/12399166/c165b8e8554a/gr1.jpg

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本文引用的文献

1
c-FLIP Protects Cardiac Microcirculation in Sepsis-Induced Myocardial Dysfunction Via FUNDC1-Mediated Regulation of Mitochondrial Autophagy.c-FLIP通过FUNDC1介导的线粒体自噬调节保护脓毒症诱导的心肌功能障碍中的心脏微循环。
JACC Basic Transl Sci. 2025 Aug;10(8):101257. doi: 10.1016/j.jacbts.2025.02.016. Epub 2025 May 14.
2
Microcirculation-driven mitochondrion dysfunction during the progression of experimental sepsis.实验性脓毒症进展过程中的微循环驱动的线粒体功能障碍。
Sci Rep. 2024 Mar 26;14(1):7153. doi: 10.1038/s41598-024-57855-9.
3
Mechanism of Mitophagy and Its Role in Sepsis Induced Organ Dysfunction: A Review.
线粒体自噬机制及其在脓毒症诱导的器官功能障碍中的作用：综述
Front Cell Dev Biol. 2021 Jun 7;9:664896. doi: 10.3389/fcell.2021.664896. eCollection 2021.
4
Crosstalk between apoptosis and autophagy signaling pathways.细胞凋亡与自噬信号通路的相互作用。
Int Rev Cell Mol Biol. 2020;352:115-158. doi: 10.1016/bs.ircmb.2020.01.003. Epub 2020 Feb 5.
5
Microcirculatory dysfunction in sepsis: pathophysiology, clinical monitoring, and potential therapies.脓毒症的微循环功能障碍：病理生理学、临床监测和潜在治疗方法。
Am J Physiol Heart Circ Physiol. 2016 Jul 1;311(1):H24-35. doi: 10.1152/ajpheart.00034.2016. Epub 2016 Apr 22.
6
Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3).制定脓毒性休克的新定义并评估新的临床标准：用于第三次脓毒症和脓毒性休克国际共识定义（Sepsis-3）。
JAMA. 2016 Feb 23;315(8):775-87. doi: 10.1001/jama.2016.0289.
7
Characterization of cardiac dysfunction in sepsis: an ongoing challenge.脓毒症心功能障碍的特征：一个持续存在的挑战。
Shock. 2014 Jan;41(1):12-24. doi: 10.1097/SHK.0000000000000065.
8
The pathways of mitophagy for quality control and clearance of mitochondria.线粒体自噬的途径：用于质量控制和线粒体清除。
Cell Death Differ. 2013 Jan;20(1):31-42. doi: 10.1038/cdd.2012.81. Epub 2012 Jun 29.
9
The microcirculation is the motor of sepsis.微循环是脓毒症的驱动因素。
Crit Care. 2005;9 Suppl 4(Suppl 4):S13-9. doi: 10.1186/cc3753. Epub 2005 Aug 25.
10
Sepsis/septic shock: participation of the microcirculation: an abbreviated review.脓毒症/脓毒性休克：微循环的参与：简要综述
Crit Care Med. 1996 Jun;24(6):1072-8. doi: 10.1097/00003246-199606000-00031.