Biochemical and biophysical research communications · 2025
Propionate alleviates diabetes-induced cardiac fibrosis in mice via regulating Serpinf1.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Bu Fangfang, Wang Yuanyuan, Li Kaiwen, Sun Hui, Yao Guihua, Zhong Jingquan, Zhang Hongyu, Lu Weida, Ji Xiaoping
Аннотация
BACKGROUND: Diabetic cardiomyopathy is a severe cardiovascular complication that adversely affects the heart health of diabetic patients. This study aims to investigate the therapeutic effects of propionate on the cardiac fibrosis phenotype in diabetic mice and to elucidate its underlying mechanisms.
METHODS: A streptozotocin-induced diabetic mouse model was used in the experiments. After successful induction of diabetes, the mice received propionate treatment. Cardiac fibrosis and inflammatory factor levels were assessed using histological analysis and biochemical assays. Furthermore, single-cell RNA sequencing and primary mouse cardiac fibroblast sequencing data were analyzed to explore the potential mechanisms underlying propionate's effects on diabetic cardiac fibrosis. Finally, the molecular mechanism by which propionate reverses diabetes-induced cardiac fibrosis was validated using shRNA knockdown experiments.
RESULTS: The results showed that propionate treatment significantly improved cardiac fibrosis in diabetic mice and reduced the levels of inflammatory factors in cardiac tissues. Additionally, propionate upregulated the expression of the Serpinf1 gene, inhibited the abnormal activation of the Wnt signaling pathway, and reduced fibrosis and marker expression levels in high-glucose-induced cardiac fibroblasts.
CONCLUSIONS: The main conclusion of this study is that propionate effectively improves the diabetic cardiac fibrosis phenotype in mice, and this therapeutic effect is specific to pathological conditions. The study further identifies Serpinf1 as the molecular target of propionate's action. These findings not only enhance our understanding of the pathophysiological mechanisms of diabetic cardiomyopathy but also provide new strategic insights for diabetes treatment, holding significant clinical application potential.
METHODS: A streptozotocin-induced diabetic mouse model was used in the experiments. After successful induction of diabetes, the mice received propionate treatment. Cardiac fibrosis and inflammatory factor levels were assessed using histological analysis and biochemical assays. Furthermore, single-cell RNA sequencing and primary mouse cardiac fibroblast sequencing data were analyzed to explore the potential mechanisms underlying propionate's effects on diabetic cardiac fibrosis. Finally, the molecular mechanism by which propionate reverses diabetes-induced cardiac fibrosis was validated using shRNA knockdown experiments.
RESULTS: The results showed that propionate treatment significantly improved cardiac fibrosis in diabetic mice and reduced the levels of inflammatory factors in cardiac tissues. Additionally, propionate upregulated the expression of the Serpinf1 gene, inhibited the abnormal activation of the Wnt signaling pathway, and reduced fibrosis and marker expression levels in high-glucose-induced cardiac fibroblasts.
CONCLUSIONS: The main conclusion of this study is that propionate effectively improves the diabetic cardiac fibrosis phenotype in mice, and this therapeutic effect is specific to pathological conditions. The study further identifies Serpinf1 as the molecular target of propionate's action. These findings not only enhance our understanding of the pathophysiological mechanisms of diabetic cardiomyopathy but also provide new strategic insights for diabetes treatment, holding significant clinical application potential.