Key result
FGF21 exerts cardioprotective effects in diabetic cardiomyopathy by mitigating fibrosis, endothelial dysfunction, and vascular smooth muscle cell abnormalities in nonmyocardial cells.
Why the study?
Recent research in diabetic cardiomyopathy has focused primarily on myocardial cells, while nonmyocardial cells also contribute significantly to pathogenesis.
This review highlights the critical role of nonmyocardial cells in the pathogenesis of diabetic cardiomyopathy and underscores the therapeutic potential of FGF21 in mitigating these specific pathological changes.
Answers are grounded in this paper and cite their sources.
Nonmyocardial cells contribute to DCM pathogenesis; extends research beyond cardiomyocytes but leaves open therapeutic targeting.
Diabetic cardiomyopathy (DCM) represents a unique myocardial disease originating from diabetic metabolic disturbances that is characterized by myocardial fibrosis and diastolic dysfunction. While recent research regarding the pathogenesis and treatment of DCM has focused primarily on myocardial cells, nonmyocardial cells-including fibroblasts, vascular smooth muscle cells (VSMCs), endothelial cells (ECs), and immune cells-also contribute significantly to the pathogenesis of DCM. Among various therapeutic targets, fibroblast growth factor 21 (FGF21) has been identified as a promising agent because of its cardioprotective effects that extend to nonmyocardial cells. In this review, we aim to elucidate the role of nonmyocardial cells in DCM and underscore the potential of FGF21 as a therapeutic strategy for these cells.
No takes yet. Share an insight, caveat, or question.
Zhang et al. (2024) conducted a review in Diabetic cardiomyopathy. Fibroblast growth factor 21 (FGF21) was evaluated. FGF21 exerts cardioprotective effects in diabetic cardiomyopathy by mitigating fibrosis, endothelial dysfunction, and vascular smooth muscle cell abnormalities in nonmyocardial cells.
Synapse has enriched 10 related papers. Consider them for comparative context: