Yixiao formula upregulated miR‐133a and inhibited TGF‐β/Smads signaling, significantly reducing myocardial fibrosis in diabetic cardiomyopathy models.
Does Yixiao formula improve myocardial fibrosis and cardiac function in a mouse model of diabetic cardiomyopathy?
Yixiao formula attenuates myocardial fibrosis and improves cardiac diastolic function in diabetic cardiomyopathy models by upregulating miR-133a and inhibiting the TGF-β/Smads signaling pathway.
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Background Yixiao formula (YXF), a traditional Chinese herbal medicine, has demonstrated clinical efficacy in alleviating symptoms of diabetic cardiomyopathy (DCM). The therapeutic mechanism underlying YXF′s effects on DCM remains poorly understood. Myocardial fibrosis is a key pathogenic mechanism in DCM, and previous studies have indicated that miR‐133a may be involved in its progression. Given that the TGF‐ β /Smads signaling pathway is a well‐established mediator of myocardial fibrosis, investigating the mechanistic role of YXF through miR‐133a and the TGF‐ β /Smads pathway warrants further exploration. Objective The main objective of this study is to investigate the potential contribution of the TGF‐ β /Smads pathway to the effects of YXF, as well as the role of miR133a, through in vivo DCM models and in vitro experiments. Materials and Methods Spontaneously diabetic KKAy mice were used to establish a DCM model by continuous high‐fat feeding, with C57BL/6 mice as controls. Echocardiography, body weight, and blood glucose data were collected every 4 weeks to examine the effects of YXF on blood glucose levels and changes in cardiac function and structure in DCM mice. Immunohistochemistry, RT‐qPCR, and western blot were used to detect the expression levels of the TGF‐ β /Smads pathway. Additionally, the potential molecular mechanism of YXF in mouse cardiac fibroblasts (MCFs) was investigated by knocking down miR‐133a. Results YXF improved fasting blood glucose levels in DCM mice, promoted cardiac diastolic function, upregulated miR133a, and inhibited the expression of the TGF‐ β /Smads pathway. Furthermore, when miR133a inhibitors were transfected under YXF intervention, we found that YXF′s inhibitory effect on the TGF‐ β /Smads pathway was weakened. Conclusion Through this study, we found that YXF can increase miR133a and inhibit the expression of the TGF‐ β /Smads pathway, thereby inhibiting myocardial fibrosis and exerting a protective effect on DCM.
Zhao et al. (Thu,) reported a other. Yixiao formula upregulated miR‐133a and inhibited TGF‐β/Smads signaling, significantly reducing myocardial fibrosis in diabetic cardiomyopathy models.