Key result
Diabetic mice exhibited significantly more severe myocardial fibrosis, apoptosis, and pyroptosis compared to controls, with increased expression of pro-apoptotic and pyroptosis-related proteins.
Why the study?
Myocardial fibrosis is an important manifestation of diabetic cardiomyopathy, but its potential mechanisms remained to be investigated.
Does hyperglycemia induce myocardial fibrosis via pyroptosis and apoptosis in diabetic mice?
Does hyperglycemia induce myocardial fibrosis via pyroptosis and apoptosis in diabetic mice?
Hyperglycemia-induced myocardial fibrosis in diabetic mice is associated with increased cardiomyocyte apoptosis and pyroptosis, suggesting potential therapeutic targets for diabetic cardiomyopathy.
Animal data implicate TGF-β1 in diabetic fibrosis; hypothesis-generating and does not inform clinical practice.
Myocardial fibrosis is an important manifestation of diabetic cardiomyopathy. This study investigated the potential mechanism of diabetic myocardial fibrosis. Male C57BL/6J and db/db mice aged 8 weeks were randomly divided into the diabetic (DB) and control groups. At 20 weeks, the mouse heart was harvested and subjected to hematoxylin-eosin staining (HE) and Masson staining to investigate the degree of fibrosis. The expressions of transforming growth factor-beta 1 (TGF-β1), collagen-III, B-cell lymphoma-2 (Bcl2), Bcl2-associated X protein (Bax), cleaved gasdermin D (GSDMD), cysteinyl aspartate specific proteinase-1 (caspase-1), apoptosis-associated speck-like protein containing a CARD (ASC), and nucleotide-binding oligomerization domain (NOD)-like receptor 3 (NLRP3) were measured by western blotting. Immunohistochemistry and TdT-mediated dUTP nick end labeling (TUNEL) staining were performed to analyze the development of apoptosis and pyroptosis. A significant increase in body weight and blood glucose in the DB group was observed. Myocardial pathological injury, fibrosis, apoptosis, and pyroptosis were more obvious and serious in the DB group. The expression of anti-apoptotic Bcl2 significantly decreased, while the expression levels of pro-apoptotic Bax, caspase-3, and pyroptosis-related proteins, such as cleaved GSDMD, and caspase-1 in the DB group were significantly increased. Pyroptosis and apoptosis were probably the main mechanisms that caused myocardial fibrosis in mice with diabetes.
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Lu et al. (2022) studied Diabetic cardiomyopathy. Diabetes (db/db model) vs. Control group (C57BL/6J mice) was evaluated on Myocardial fibrosis, apoptosis, and pyroptosis. Diabetic mice exhibited significantly more severe myocardial fibrosis, apoptosis, and pyroptosis compared to controls, with increased expression of pro-apoptotic and pyroptosis-related proteins.
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