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缺氧诱导肺动脉平滑肌细胞表型转化机制的研究进展。

Research progress on the mechanism of phenotypic transformation of pulmonary artery smooth muscle cells induced by hypoxia.

机构信息

1. Medical Institute of Qinghai University, Xining 810001, China.

2. Research Center for High Altitude Medicine, Qinghai University, Xining 810001, China.

出版信息

Zhejiang Da Xue Xue Bao Yi Xue Ban. 2022 Dec 25;51(6):750-757. doi: 10.3724/zdxbyxb-2022-0282.

Abstract

Phenotypic transformation of pulmonary artery smooth muscle cells (PASMCs) is a key factor in pulmonary vascular remodeling. Inhibiting or reversing phenotypic transformation can inhibit pulmonary vascular remodeling and control the progression of hypoxic pulmonary hypertension. Recent studies have shown that hypoxia causes intracellular peroxide metabolism to induce oxidative stress, induces multi-pathway signal transduction, including those related to autophagy, endoplasmic reticulum stress and mitochondrial dysfunction, and also induces non-coding RNA regulation of cell marker protein expression, resulting in PASMCs phenotypic transformation. This article reviews recent research progress on mechanisms of hypoxia-induced phenotypic transformation of PASMCs, which may be helpful for finding targets to inhibit phenotypic transformation and to improve pulmonary vascular remodeling diseases such as hypoxia-induced pulmonary hypertension.

摘要

肺血管平滑肌细胞(PASMCs)的表型转化是肺血管重构的关键因素。抑制或逆转表型转化可以抑制肺血管重构,控制低氧性肺动脉高压的进展。最近的研究表明,低氧导致细胞内过氧化物代谢引起氧化应激,诱导多途径信号转导,包括与自噬、内质网应激和线粒体功能障碍相关的信号转导,还诱导细胞标记蛋白表达的非编码 RNA 调控,导致 PASMCs 的表型转化。本文综述了近年来低氧诱导 PASMCs 表型转化机制的研究进展,这可能有助于寻找抑制表型转化的靶点,改善低氧性肺动脉高压等肺血管重构疾病。

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