病理心肌肥厚中的转化生长因子-β和骨形态发生蛋白信号通路

IF 3.4 3区 生物学 Q3 CELL BIOLOGY Cell Cycle Pub Date : 2023-11-01 Epub Date: 2024-01-18 DOI:10.1080/15384101.2023.2293595
Jing Wen, Guixiang Liu, Mingjie Liu, Huarui Wang, Yunyan Wan, Zhouhong Yao, Nannan Gao, Yuanyuan Sun, Ling Zhu
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引用次数: 0

摘要

病理性心脏肥大(简称心肌肥大)是心脏对各种病理刺激的不良反应,心肌肥大是心力衰竭和猝死的独立危险因素。目前,治疗心脏肥大的方法仅限于改善症状,效果甚微。从分子水平上阐明心脏肥大的发展过程并确定治疗心脏肥大的新靶点至关重要。在这篇综述中,我们总结了与心肌肥大发病机制相关的多种活性物质及其信号通路的研究,重点关注转化生长因子-β(TGF-β)和骨形态发生蛋白(BMP)信号在心肌肥大发展过程中的作用,以及确定潜在的分子干预靶点。我们的目标是找出具有临床价值的重要信号分子,希望有助于促进心脏肥大的精确治疗,从而改善患者的预后。
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Transforming growth factor-β and bone morphogenetic protein signaling pathways in pathological cardiac hypertrophy.

Pathological cardiac hypertrophy (referred to as cardiac hypertrophy) is a maladaptive response of the heart to a variety of pathological stimuli, and cardiac hypertrophy is an independent risk factor for heart failure and sudden death. Currently, the treatments for cardiac hypertrophy are limited to improving symptoms and have little effect. Elucidation of the developmental process of cardiac hypertrophy at the molecular level and the identification of new targets for the treatment of cardiac hypertrophy are crucial. In this review, we summarize the research on multiple active substances related to the pathogenesis of cardiac hypertrophy and the signaling pathways involved and focus on the role of transforming growth factor-β (TGF-β) and bone morphogenetic protein (BMP) signaling in the development of cardiac hypertrophy and the identification of potential targets for molecular intervention. We aim to identify important signaling molecules with clinical value and hope to help promote the precise treatment of cardiac hypertrophy and thus improve patient outcomes.

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来源期刊
Cell Cycle
Cell Cycle 生物-细胞生物学
CiteScore
7.70
自引率
2.30%
发文量
281
审稿时长
1 months
期刊介绍: Cell Cycle is a bi-weekly peer-reviewed journal of high priority research from all areas of cell biology. Cell Cycle covers all topics from yeast to man, from DNA to function, from development to aging, from stem cells to cell senescence, from metabolism to cell death, from cancer to neurobiology, from molecular biology to therapeutics. Our goal is fast publication of outstanding research.
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