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Role of PI3K/Akt signaling pathway in cardiac fibrosis
Molecular and Cellular Biochemistry ( IF 3.5 ) Pub Date : 2021-07-10 , DOI: 10.1007/s11010-021-04219-w
Wuming Qin 1 , Linghui Cao 2 , Isaac Yaw Massey 3
Affiliation  

Heart failure (HF) is considered as a severe health problem worldwide, while cardiac fibrosis is one of the main driving factors for the progress of HF. Cardiac fibrosis was characterized by changes in cardiomyocytes, cardiac fibroblasts, ratio of collagen (COL) I/III, and the excessive production and deposition of extracellular matrix (ECM), thus forming a scar tissue, which leads to pathological process of cardiac structural changes and systolic as well as diastolic dysfunction. Cardiac fibrosis is a common pathological change of many advanced cardiovascular diseases including ischemic heart disease, hypertension, and HF. Accumulated studies have proven that phosphoinositol-3 kinase (PI3K)/Akt signaling pathway is involved in regulating the occurrence, progression and pathological formation of cardiac fibrosis via regulating cell survival, apoptosis, growth, cardiac contractility and even the transcription of related genes through a series of molecules including mammalian target of rapamycin (mTOR), glycogen synthase kinase 3 (GSK-3), forkhead box proteins O1/3 (FoxO1/3), and nitric oxide synthase (NOS). Thus, the review focuses on the role of PI3K/Akt signaling pathway in the cardiac fibrosis. The information reviewed here should be significant in understanding the role of PI3K/Akt in cardiac fibrosis and contribute to the design of further studies related to PI3K/Akt and the cardiac fibrotic response, as well as sought to shed light on a potential treatment for cardiac fibrosis.



中文翻译:

PI3K/Akt信号通路在心脏纤维化中的作用

心力衰竭(HF)在世界范围内被认为是一个严重的健康问题,而心脏纤维化是心力衰竭进展的主要驱动因素之一。心脏纤维化的特点是心肌细胞、心脏成纤维细胞、胶原蛋白(COL)I/III比值发生改变,细胞外基质(ECM)过度生成和沉积,从而形成瘢痕组织,导致心脏结构改变的病理过程和收缩和舒张功能障碍。心脏纤维化是许多晚期心血管疾病的常见病理变化,包括缺血性心脏病、高血压和心力衰竭。积累的研究证明,磷酸肌醇3激酶(PI3K)/Akt信号通路通过调节细胞存活,参与调控心脏纤维化的发生、发展和病理形成,通过一系列分子包括哺乳动物雷帕霉素靶蛋白 (mTOR)、糖原合酶激酶 3 (GSK-3)、叉头盒蛋白 O1/3 (FoxO1/3) 和一氧化氮合酶(NOS)。因此,本综述重点关注 PI3K/Akt 信号通路在心脏纤维化中的作用。此处审查的信息对于了解 PI3K/Akt 在心脏纤维化中的作用具有重要意义,有助于设计与 PI3K/Akt 和心脏纤维化反应相关的进一步研究,并试图阐明心脏的潜在治疗方法纤维化。叉头盒蛋白 O1/3 (FoxO1/3) 和一氧化氮合酶 (NOS)。因此,本综述重点关注 PI3K/Akt 信号通路在心脏纤维化中的作用。此处审查的信息对于了解 PI3K/Akt 在心脏纤维化中的作用具有重要意义,有助于设计与 PI3K/Akt 和心脏纤维化反应相关的进一步研究,并试图阐明心脏的潜在治疗方法纤维化。叉头盒蛋白 O1/3 (FoxO1/3) 和一氧化氮合酶 (NOS)。因此,本综述重点关注 PI3K/Akt 信号通路在心脏纤维化中的作用。此处回顾的信息对于理解 PI3K/Akt 在心脏纤维化中的作用具有重要意义,有助于设计与 PI3K/Akt 和心脏纤维化反应相关的进一步研究,并寻求阐明潜在的心脏治疗方法纤维化。

更新日期:2021-07-10
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