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血管平滑肌 PPARγ的抗炎机制。

Anti-inflammatory mechanisms of the vascular smooth muscle PPARγ.

机构信息

Laboratory of Veterinary Pharmacology, Faculty of Veterinary Medicine, Okayama University of Science, Imabari, Ehime 794-8555, Japan.

出版信息

J Smooth Muscle Res. 2021;57(0):1-7. doi: 10.1540/jsmr.57.1.

DOI:10.1540/jsmr.57.1
PMID:33658456
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7920819/
Abstract

This review highlights molecular mechanisms of anti-inflammatory and protective effects of the nuclear transcription factor, peroxisome proliferator-activated receptor γ (PPARγ) in vascular tissue. PPARγ is an ubiquitously expressed nuclear factor, and well-studied in adipose tissue and inflammatory cells. Additionally, beneficial effects of vascular PPARγ's on atherosclerosis and vascular remodeling/dysfunction have been reported although the detailed mechanism remains to be completely elucidated. Clinical and basic studies have shown that the synthetic PPARγ ligands, thiazolidinediones (TZDs), have protective effects against cardiovascular diseases such as atherosclerosis. Recent studies utilizing genetic tools suggested that those protective effects of TZDs on cardiovascular diseases are not due to a consequence of improvement of insulin resistance, but may be due to a direct effect on PPARγ's in vascular endothelial and smooth muscle cells. In this review, we discuss proposed mechanisms by which the vascular PPARγ regulates vascular inflammation and remodeling/dysfunction especially in smooth muscle cells.

摘要

这篇综述强调了核转录因子过氧化物酶体增殖物激活受体 γ(PPARγ)在血管组织中抗炎和保护作用的分子机制。PPARγ 是一种广泛表达的核因子,在脂肪组织和炎症细胞中研究得较多。此外,尽管详细的机制仍有待完全阐明,但已有研究报道血管 PPARγ 对动脉粥样硬化和血管重塑/功能障碍有有益作用。临床和基础研究表明,合成的 PPARγ 配体噻唑烷二酮(TZDs)对动脉粥样硬化等心血管疾病具有保护作用。最近利用遗传工具的研究表明,TZDs 对心血管疾病的这些保护作用不是由于改善胰岛素抵抗的结果,而是可能由于对血管内皮和平滑肌细胞中 PPARγ 的直接作用。在这篇综述中,我们讨论了血管 PPARγ 调节血管炎症和重塑/功能障碍的机制,特别是在平滑肌细胞中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e472/7920819/ab8c56e2f6f9/jsmr-57-001-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e472/7920819/ab8c56e2f6f9/jsmr-57-001-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e472/7920819/ab8c56e2f6f9/jsmr-57-001-g001.jpg

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PPARγ and RhoBTB1 in hypertension.过氧化物酶体增殖物激活受体γ 和 RhoBTB1 与高血压。
Curr Opin Nephrol Hypertens. 2020 Mar;29(2):161-170. doi: 10.1097/MNH.0000000000000579.
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Conditional deletion of smooth muscle Cullin-3 causes severe progressive hypertension.平滑肌 Cullin-3 条件性缺失导致严重进行性高血压。
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LRP1 Deficiency in Vascular SMC Leads to Pulmonary Arterial Hypertension That Is Reversed by PPARγ Activation.LRP1 缺失导致血管平滑肌细胞肺动脉高压,PPARγ 激活可逆转该疾病。
PPARγ Agonist Rosiglitazone and Antagonist GW9662: Antihypertensive Effects on Chronic Intermittent Hypoxia-Induced Hypertension in Rats.
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Drugs Interfering with Insulin Resistance and Their Influence on the Associated Hypermetabolic State in Severe Burns: A Narrative Review.药物干预胰岛素抵抗及其对严重烧伤相关高代谢状态的影响:叙述性综述。
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