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心肌重塑中烟酰胺腺嘌呤二核苷酸磷酸氧化酶的研究进展

Advances in the study of nicotinamide adenine dinucleotide phosphate oxidase in myocardial remodeling.

作者信息

Miao Runran, Wang Libo, Chen Zhigang, Ge Shiqi, Li Li, Zhang Kai, Chen Yingen, Guo Wenjing, Duan Xulei, Zhu Mingyang, Zhao Guoan, Lin Fei

机构信息

Department of Cardiology, The First Affiliated Hospital of Xinxiang Medical University, Heart Center of Xinxiang Medical University, Xinxiang, China.

College of Chemistry and Chemical Engineering, Henan Normal University, Xinxiang, China.

出版信息

Front Cardiovasc Med. 2022 Nov 3;9:1000578. doi: 10.3389/fcvm.2022.1000578. eCollection 2022.

DOI:10.3389/fcvm.2022.1000578
PMID:36407440
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9669076/
Abstract

Myocardial remodeling is a key pathophysiological basis of heart failure, which seriously threatens human health and causes a severe economic burden worldwide. During chronic stress, the heart undergoes myocardial remodeling, mainly manifested by cardiomyocyte hypertrophy, apoptosis, interstitial fibrosis, chamber enlargement, and cardiac dysfunction. The NADPH oxidase family (NOXs) are multisubunit transmembrane enzyme complexes involved in the generation of redox signals. Studies have shown that NOXs are highly expressed in the heart and are involved in the pathological development process of myocardial remodeling, which influences the development of heart failure. This review summarizes the progress of research on the pathophysiological processes related to the regulation of myocardial remodeling by NOXs, suggesting that NOXs-dependent regulatory mechanisms of myocardial remodeling are promising new therapeutic targets for the treatment of heart failure.

摘要

心肌重构是心力衰竭的关键病理生理基础,严重威胁人类健康并在全球造成沉重的经济负担。在慢性应激过程中,心脏会发生心肌重构,主要表现为心肌细胞肥大、凋亡、间质纤维化、心腔扩大和心脏功能障碍。NADPH氧化酶家族(NOXs)是参与氧化还原信号产生的多亚基跨膜酶复合物。研究表明,NOXs在心脏中高度表达,并参与心肌重构的病理发展过程,影响心力衰竭的发生发展。本文综述了NOXs对心肌重构调节相关病理生理过程的研究进展,提示NOXs依赖的心肌重构调节机制有望成为治疗心力衰竭的新治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b858/9669076/c3e24fe92e03/fcvm-09-1000578-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b858/9669076/2df51c4a90b5/fcvm-09-1000578-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b858/9669076/a1e62e6ac483/fcvm-09-1000578-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b858/9669076/c3e24fe92e03/fcvm-09-1000578-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b858/9669076/2df51c4a90b5/fcvm-09-1000578-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b858/9669076/a1e62e6ac483/fcvm-09-1000578-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b858/9669076/c3e24fe92e03/fcvm-09-1000578-g003.jpg

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Telomere Shortening in Hypertensive Heart Disease Depends on Oxidative DNA Damage and Predicts Impaired Recovery of Cardiac Function in Heart Failure.高血压性心脏病中的端粒缩短取决于氧化 DNA 损伤,并预测心力衰竭中心脏功能恢复受损。
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SERCA2a dysfunction in the pathophysiology of heart failure with preserved ejection fraction: a direct role is yet to be established.射血分数保留的心力衰竭病理生理学中的肌浆网Ca2+-ATP酶2a功能障碍:直接作用尚未确立。
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