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IF 2.6 3区生物学 Q2 GENETICS & HEREDITY

Gene Pub Date : 2025-03-13 DOI:10.1016/j.gene.2025.149418

Zhen Gao

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引用次数: 0

摘要

心肌组织受损导致心肌纤维化是各种心脏疾病的重要病理标志。SMAD3 是转化生长因子-β（TGF-β）信号通路中的一个核心转录调节因子，在心肌纤维化和心脏重塑的病理过程中起着关键作用。它错综复杂地调节着细胞增殖、分化、组织修复和纤维化等生理和病理过程。值得注意的是，SMAD3 在心肌梗死后的心肌纤维化、压力过载诱导的心肌纤维化、糖尿病心肌病（DCM）、衰老相关的心肌纤维化和心肌炎相关的心肌纤维化中发挥着至关重要的影响。有针对性地调节基因或利用包括中药（芍药苷、黄芩苷和染料木苷等）在内的化合物以及其他调节 SMAD3 的药物制剂，可为抑制心肌纤维化的病理级联反应提供途径。因此，有针对性地调节与心肌纤维化相关的 SMAD3 可能预示着改善心肌疾病的新治疗范例。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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New insights into Smad3 in cardiac fibrosis

Damage to myocardial tissues, leading to myocardial fibrosis, is a significant pathological hallmark across various heart diseases. SMAD3, a central transcriptional regulator within the transforming growth factor-beta (TGF-β) signaling pathway, plays a pivotal role in the pathological progression of myocardial fibrosis and cardiac remodeling. It intricately regulates physiological and pathological processes encompassing cell proliferation, differentiation, tissue repair, and fibrosis. Notably, SMAD3 exerts crucial influences in myocardial fibrosis subsequent to myocardial infarction, pressure overload-induced myocardial fibrosis, diabetic cardiomyopathy (DCM), aging-associated cardiac fibrosis and myocarditis-related myocardial fibrosis. The targeted modulation of genes or the utilization of compounds, including traditional Chinese medicine (paeoniflorin, baicalin, and genistein et al.) and other pharmaceutical agents that modulate SMAD3, may offer avenues for restraining the pathological cascade of myocardial fibrosis. Consequently, targeted regulation of SMAD3 associated with myocardial fibrosis may herald novel therapeutic paradigms for ameliorating myocardial diseases.

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来源期刊

Gene 生物-遗传学

CiteScore

6.10

自引率

2.90%

发文量

718

审稿时长

42 days

期刊介绍： Gene publishes papers that focus on the regulation, expression, function and evolution of genes in all biological contexts, including all prokaryotic and eukaryotic organisms, as well as viruses.