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过氧化物酶体增殖物激活受体γ对心脏纤维化至关重要。

Peroxisome Proliferator-Activated Receptor-γ Is Critical to Cardiac Fibrosis.

作者信息

Liu Huang-Jun, Liao Hai-Han, Yang Zheng, Tang Qi-Zhu

机构信息

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China; Hubei Key Laboratory of Cardiology, Wuhan 430060, China.

出版信息

PPAR Res. 2016;2016:2198645. doi: 10.1155/2016/2198645. Epub 2016 May 12.

DOI:10.1155/2016/2198645
PMID:27293418
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4880703/
Abstract

Peroxisome proliferator-activated receptor-γ (PPARγ) is a ligand-activated transcription factor belonging to the nuclear receptor superfamily, which plays a central role in regulating lipid and glucose metabolism. However, accumulating evidence demonstrates that PPARγ agonists have potential to reduce inflammation, influence the balance of immune cells, suppress oxidative stress, and improve endothelial function, which are all involved in the cellular and molecular mechanisms of cardiac fibrosis. Thus, in this review we discuss the role of PPARγ in various cardiovascular conditions associated with cardiac fibrosis, including diabetes mellitus, hypertension, myocardial infarction, heart failure, ischemia/reperfusion injury, atrial fibrillation, and several other cardiovascular disease (CVD) conditions, and summarize the developmental status of PPARγ agonists for the clinical management of CVD.

摘要

过氧化物酶体增殖物激活受体γ(PPARγ)是一种属于核受体超家族的配体激活转录因子,在调节脂质和葡萄糖代谢中起核心作用。然而,越来越多的证据表明,PPARγ激动剂具有减轻炎症、影响免疫细胞平衡、抑制氧化应激以及改善内皮功能的潜力,而这些均参与了心脏纤维化的细胞和分子机制。因此,在本综述中,我们讨论了PPARγ在与心脏纤维化相关的各种心血管疾病中的作用,包括糖尿病、高血压、心肌梗死、心力衰竭、缺血/再灌注损伤、心房颤动以及其他几种心血管疾病(CVD)情况,并总结了用于CVD临床管理的PPARγ激动剂的发展现状。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45d/4880703/450abaf914f7/PPAR2016-2198645.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45d/4880703/4d18c1bd5b00/PPAR2016-2198645.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45d/4880703/450abaf914f7/PPAR2016-2198645.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45d/4880703/4d18c1bd5b00/PPAR2016-2198645.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45d/4880703/450abaf914f7/PPAR2016-2198645.002.jpg

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PPAR Res. 2015;2015:271983. doi: 10.1155/2015/271983. Epub 2015 Oct 26.
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PEDF and 34-mer inhibit angiogenesis in the heart by inducing tip cells apoptosis via up-regulating PPAR-γ to increase surface FasL.色素上皮衍生因子(PEDF)和34肽通过上调过氧化物酶体增殖物激活受体γ(PPAR-γ)以增加表面Fas配体(FasL),诱导尖端细胞凋亡,从而抑制心脏血管生成。
Apoptosis. 2016 Jan;21(1):60-8. doi: 10.1007/s10495-015-1186-1.
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Fibrosis, Connexin-43, and Conduction Abnormalities in the Brugada Syndrome.
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bioRxiv. 2024 Dec 12:2024.12.06.627231. doi: 10.1101/2024.12.06.627231.
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