This study demonstrates kaempferol's ability to improve cardiac function in mice with myocardial fibrosis, suggesting reduced inflammation and downregulation of coagulation factor VII.
Myocardial fibrosis is a critical pathological process in the progression of heart failure and other cardiovascular diseases. Kaempferol (KMP), a natural flavonoid, has antioxidant and anti-inflammatory properties. This study investigates the effects of KMP on myocardial fibrosis. Isoproterenol injection was used to establish myocardial fibrosis mouse model. Cardiac function was assessed by echocardiography. Histology analysis was conducted using Masson assay and Sirius red staining. The expression of survival of motor neuron 1 (α-SMA) and Collagen III was detected using immunohistochemistry. RNA expression was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cytokine release was detected using enzyme-linked immunosorbent assay. Protein expression was detected using Western blot. We found that KMP treatment improved cardiac function as well as suppressed myocardial fibrosis. Moreover, KMP treatment decreased expression of fibrosis-related genes and attenuated inflammation in fibrotic hearts. Furthermore, KMP treatment inhibited the expression of coagulation factor VII (FVII), the overexpression of which promoted inflammation response and myocardial fibrosis. In summary, KMP exerts protective effects against myocardial fibrosis via downregulating FVII. These findings suggest that KMP may be a promising therapeutic candidate for myocardial fibrosis.
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Zhang et al. (2025) studied this question.
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