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Review
. 2024 Sep 26;22(1):446.
doi: 10.1186/s12964-024-01842-0.

The role of nonmyocardial cells in the development of diabetic cardiomyopathy and the protective effects of FGF21: a current understanding

Tianyi Zhang #  1 , Donghui Jiang #  1 , Xiao Zhang  1 , Ligang Chen  2 , Jun Jiang  3   4 , Chunxiang Zhang  5   6 , Shengbiao Li  7   8 , Qiuhong Li  9
Affiliations
Review

The role of nonmyocardial cells in the development of diabetic cardiomyopathy and the protective effects of FGF21: a current understanding

Tianyi Zhang et al. Cell Commun Signal. .

Abstract

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.

Keywords: Diabetic cardiomyopathy; Fibroblast growth factor 21; Nonmyocardial cells.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Contribution of nonmyocardial cells to the development of DCM
Fig. 2
Fig. 2
Role of CFs in DCM and the corresponding protective effects of FGF21
Fig. 3
Fig. 3
Role of endothelial dysfunction in DCM and the corresponding protective effects of FGF21
Fig. 4
Fig. 4
Role of cardiac VSMC dysfunction in DCM and the corresponding protective effects of FGF21
Fig. 5
Fig. 5
Role of immune cell activation in DCM and the corresponding protective effects of FGF21
See this image and copyright information in PMC

References

    1. Schleicher E, Gerdes C, Petersmann A, Müller-Wieland D, Müller UA, Freckmann G, et al. Definition, classification and diagnosis of diabetes mellitus. Exp Clin Endocrinol Diabetes. 2022;130:S1-8. - PubMed
    1. Atlas D. International diabetes federation. In: IDF Diabetes Atlas, 7th edn. Brussels: International Diabetes Federation. 2015. p. 33.
    1. Abraham TM, Pencina KM, Pencina MJ, Fox CS. Trends in diabetes incidence: the Framingham Heart Study. Diabetes Care. 2015;38:482–7. - PMC - PubMed
    1. Rubler S, Dlugash J, Yuceoglu YZ, Kumral T, Branwood AW, Grishman A. New type of cardiomyopathy associated with diabetic glomerulosclerosis. Am J Cardiol. 1972;30:595–602. - PubMed
    1. Cai L, Li W, Wang G, Guo L, Jiang Y, Kang YJ. Hyperglycemia-induced apoptosis in mouse myocardium: mitochondrial cytochrome C-mediated caspase-3 activation pathway. Diabetes. 2002;51:1938–48. - PubMed

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