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A Mighty Mitochondrial Microprotein: The Protective Role of MOTS-c in Acute Lung Injury.

作者信息

Kliment Corrine

机构信息

Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania.

出版信息

Am J Respir Cell Mol Biol. 2025 Sep;73(3):335-336. doi: 10.1165/rcmb.2025-0062ED.

DOI:10.1165/rcmb.2025-0062ED
PMID:40072017
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12416303/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22c6/12416303/07e1d7a6afd4/rcmb.2025-0062EDf1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22c6/12416303/07e1d7a6afd4/rcmb.2025-0062EDf1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22c6/12416303/07e1d7a6afd4/rcmb.2025-0062EDf1.jpg

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A Mighty Mitochondrial Microprotein: The Protective Role of MOTS-c in Acute Lung Injury.一种强大的线粒体微小蛋白:MOTS-c在急性肺损伤中的保护作用。
Am J Respir Cell Mol Biol. 2025 Sep;73(3):335-336. doi: 10.1165/rcmb.2025-0062ED.
2
MOTS-c Promotes Glycolysis via AMPK-HIF-1α-PFKFB3 Pathway to Ameliorate CPB-induced Lung Injury.心肌代谢物-胱抑素C通过AMPK-HIF-1α-PFKFB3途径促进糖酵解以改善体外循环诱导的肺损伤。
Am J Respir Cell Mol Biol. 2025 Mar 4. doi: 10.1165/rcmb.2024-0533OC.
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本文引用的文献

1
MOTS-c Promotes Glycolysis via AMPK-HIF-1α-PFKFB3 Pathway to Ameliorate CPB-induced Lung Injury.心肌代谢物-胱抑素C通过AMPK-HIF-1α-PFKFB3途径促进糖酵解以改善体外循环诱导的肺损伤。
Am J Respir Cell Mol Biol. 2025 Mar 4. doi: 10.1165/rcmb.2024-0533OC.
2
The role of FPR2-mediated ferroptosis in formyl peptide-induced acute lung injury against endothelial barrier damage and protective effect of the mitochondria-derived peptide MOTS-c.FPR2 介导线粒体铁死亡在甲酰肽诱导的急性肺损伤对抗内皮屏障损伤中的作用及线粒体来源肽 MOTS-c 的保护作用。
Int Immunopharmacol. 2024 Apr 20;131:111911. doi: 10.1016/j.intimp.2024.111911. Epub 2024 Mar 24.
3
Alterations in circulating mitochondrial signals at hospital admission for COPD exacerbation.
慢性阻塞性肺疾病(COPD)加重住院时循环线粒体信号的改变。
Chron Respir Dis. 2023 Jan-Dec;20:14799731231220058. doi: 10.1177/14799731231220058.
4
Mitochondrial microproteins: critical regulators of protein import, energy production, stress response pathways, and programmed cell death.线粒体小蛋白:蛋白输入、能量产生、应激反应途径和程序性细胞死亡的关键调节因子。
Am J Physiol Cell Physiol. 2023 Oct 1;325(4):C807-C816. doi: 10.1152/ajpcell.00189.2023. Epub 2023 Aug 29.
5
The mitochondrial-derived peptide MOTS-c suppresses ferroptosis and alleviates acute lung injury induced by myocardial ischemia reperfusion via PPARγ signaling pathway.线粒体衍生肽 MOTS-c 通过 PPARγ 信号通路抑制铁死亡,减轻心肌缺血再灌注引起的急性肺损伤。
Eur J Pharmacol. 2023 Aug 15;953:175835. doi: 10.1016/j.ejphar.2023.175835. Epub 2023 Jun 7.
6
Associations between serum mitokine levels and outcomes in stable COPD: an observational prospective study.稳定期 COPD 患者血清线粒体因子水平与结局的相关性:一项观察性前瞻性研究。
Sci Rep. 2022 Oct 15;12(1):17315. doi: 10.1038/s41598-022-21757-5.
7
MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis.MOTS-c 是一种运动诱导的线粒体编码调节因子,可调节与年龄相关的身体衰退和肌肉内稳态。
Nat Commun. 2021 Jan 20;12(1):470. doi: 10.1038/s41467-020-20790-0.
8
Protective effect of MOTS-c on acute lung injury induced by lipopolysaccharide in mice.MOTS-c 对脂多糖诱导的小鼠急性肺损伤的保护作用。
Int Immunopharmacol. 2020 Mar;80:106174. doi: 10.1016/j.intimp.2019.106174. Epub 2020 Jan 10.
9
The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.线粒体衍生肽MOTS-c可促进代谢稳态,减轻肥胖和胰岛素抵抗。
Cell Metab. 2015 Mar 3;21(3):443-54. doi: 10.1016/j.cmet.2015.02.009.
10
Subphenotypes in acute respiratory distress syndrome: latent class analysis of data from two randomised controlled trials.急性呼吸窘迫综合征的亚表型:两项随机对照试验数据的潜在类别分析。
Lancet Respir Med. 2014 Aug;2(8):611-20. doi: 10.1016/S2213-2600(14)70097-9. Epub 2014 May 19.