Kolling Institute for Medical Research, Royal North Shore Hospital, St Leonards 2065, Australia.
Faculty of Medicine and Health, The University of Sydney, St Leonards 2065, Australia.
Int J Mol Sci. 2020 Feb 1;21(3):970. doi: 10.3390/ijms21030970.
Diabetic cardiomyopathy involves remodeling of the heart in response to diabetes that includes microvascular damage, cardiomyocyte hypertrophy, and cardiac fibrosis. Cardiac fibrosis is a major contributor to diastolic dysfunction that can ultimately result in heart failure with preserved ejection fraction. Cardiac fibroblasts are the final effector cell in the process of cardiac fibrosis. This review article aims to describe the cardiac fibroblast phenotype in response to high-glucose conditions that mimic the diabetic state, as well as to explain the pathways underlying this phenotype. As such, this review focuses on studies conducted on isolated cardiac fibroblasts. We also describe molecules that appear to oppose the pro-fibrotic actions of high glucose on cardiac fibroblasts. This represents a major gap in knowledge in the field that needs to be addressed.
糖尿病性心肌病涉及心脏对糖尿病的重塑反应,包括微血管损伤、心肌细胞肥大和心脏纤维化。心脏纤维化是舒张功能障碍的主要原因,最终可导致射血分数保留的心力衰竭。心脏成纤维细胞是心脏纤维化过程中的终末效应细胞。这篇综述文章旨在描述心脏成纤维细胞在高糖条件下的表型,这些条件模拟糖尿病状态,并解释这种表型背后的途径。因此,本综述重点介绍了在分离的心脏成纤维细胞上进行的研究。我们还描述了一些似乎对抗高糖对心脏成纤维细胞的促纤维化作用的分子。这是该领域需要解决的一个重大知识空白。