细胞生物学
再生(生物学)
心肌细胞
血管生成
压电1
斑马鱼
生物
PI3K/AKT/mTOR通路
信号转导
内科学
医学
癌症研究
离子通道
受体
机械敏感通道
生物化学
基因
作者
Khalid Saad Alharbi,Waleed Hassan Almalki,Sami I. Alzarea,Imran Kazmi,Fahad A. Al‐Abbasi,Obaid Afzal,Abdulmalik Saleh Alfawaz Altamimi,Sachin Kumar Singh,Kamal Dua,Gaurav Gupta
标识
DOI:10.1016/j.cbi.2022.110011
摘要
Cardiomyocyte regeneration following cardiac damage is challenging to study because of the inflammatory process, the multiplication of cells in the stroma, and the creation of scar tissue. In addition to the initial damage, the subsequent decrease in cardiac myocytes adds to heart failure. Piezo1 is remarkably understudied in the heart, which may be related to its recent discovery. Despite this, Piezo1 is expressed in a variety of cardiovascular cell populations, notably epithelial cells (EC), cardiac fibroblasts (CF), and cardiac myocytes (CM), in both animal and human samples, with fibroblasts expressing more than myocytes. Researchers have recently shown that disrupting Piezo1 signaling causes defects in zebrafish developing the outflow tract (OFT) and aortic valves. Platelet plasma membranes may provide lipid substrates, such as phosphatidylinositol bisphosphate, that aid in activating the piezo 1 ion channel in the cardiovascular system. In addition, CXC chemokine ligand 8/CXC chemokine receptor 1/2 (CXCL8-CXCR1/2) signaling was identified to establish the proliferation of coronary endothelial cells during cardiac regeneration. Notably, all these pathways are calcium-dependent, and cell proliferation and angiogenesis were necessary to recover myocardial cells. This review will examine the most current findings to understand further how platelet-rich plasma (PRP) and the piezo 1 channel might aid in cardiomyocyte regeneration.
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