Role of TRPM7 in cardiac fibrosis: A potential therapeutic target (Review).
Role of TRPM7 in cardiac fibrosis: A potential therapeutic target (Review).
复制标题
DOI：
10.3892/etm.2020.9604
复制
发表时间：
2021-03
影响因子：
2.7
通讯作者：
Cheng X
中科院分区：
文献类型：
--
作者：
Hu F;Li M;Han F;Zhang Q;Zeng Y;Zhang W;Cheng X
心脏纤维化是心脏重塑的标志，几乎与所有形式的心脏病相关。由于心脏纤维化的病因和发病机制复杂多样，临床上尚无有效的治疗药物。TRPM 7是一种二合一的蛋白质结构，其普遍存在的表达谱和独特的生物物理学特性使得TRPM 7能够参与纤维化相关心脏疾病的发病机制和发展，如心力衰竭（HF）、心肌病、心律失常和醛固酮增多症。多种生物活性分子对多种刺激的反应可以激活TRPM 7和相关信号通路，导致心脏成纤维细胞增殖、分化和细胞外基质产生。TRPM 7介导的Ca 2+信号通路和TGF-β1信号通路对于纤维化的形成至关重要。越来越多的证据表明，TRPM 7是阻止纤维化心脏疾病发展的潜在药理学靶点。目前迫切需要可靠的类药物分子，用于进一步开发靶向TRPM 7的高亲和力体内药物。本综述讨论了TRPM 7在心脏纤维化中的广泛和重要作用，并重点关注其作为缓解心脏纤维化的治疗靶点的潜力。
Cardiac fibrosis is a hallmark of cardiac remodeling associated with nearly all forms of heart disease. Clinically, no effective therapeutic drugs aim to inhibit cardiac fibrosis, owing to the complex etiological heterogeneity and pathogenesis of this disease. A two-in-one protein structure, a ubiquitous expression profile and unique biophysical characteristics enable the involvement of transient receptor potential melastatin-subfamily member 7 (TRPM7) in the pathogenesis and development of fibrosis-related cardiac diseases, such as heart failure (HF), cardiomyopathies, arrhythmia and hyperaldosteronism. In response to a variety of stimuli, multiple bioactive molecules can activate TRPM7 and related signaling pathways, leading to fibroblast proliferation, differentiation and extracellular matrix production in cardiac fibroblasts. TRPM7-mediated Ca2+ signaling and TGF-β1 signaling pathways are critical for the formation of fibrosis. Accumulating evidence has demonstrated that TRPM7 is a potential pharmacological target for halting the development of fibrotic cardiac diseases. Reliable drug-like molecules for further development of high-affinity in vivo drugs targeting TRPM7 are urgently needed. The present review discusses the widespread and significant role of TRPM7 in cardiac fibrosis and focuses on its potential as a therapeutic target for alleviating heart fibrogenesis.
登录
查看更多内容
DOI：
10.1186/1755-1536-5-15
发表时间：
2012-09-03
期刊：
Fibrogenesis & tissue repair
影响因子：
--
作者：
Fan D;Takawale A;Lee J;Kassiri Z
通讯作者：
Kassiri Z
影响因子：
9.8
作者：
Baldoli, Erika;Maier, Jeanette A. M.
通讯作者：
Maier, Jeanette A. M.
影响因子：
3.2
作者：
Altura, BM;Kostellow, AB;Altura, BT
通讯作者：
Altura, BT
影响因子：
3.5
作者：
Clark, Kristopher;Middelbeek, Jeroen;van Leeuwen, Frank N.
通讯作者：
van Leeuwen, Frank N.
影响因子：
2.8
作者：
Demir, Tuncer;Yumrutas, Onder;Bagci, Cahit
通讯作者：
Bagci, Cahit