Key result
Deletion of IL-6 significantly improved cardiac function and alleviated interstitial fibrosis in streptozotocin-induced diabetic mice compared to wild-type diabetic mice.
Why the study?
Does IL-6 deletion improve cardiac function and alleviate interstitial fibrosis in a mouse model of diabetic cardiomyopathy?
Does IL-6 deletion improve cardiac function and alleviate interstitial fibrosis in a mouse model of diabetic cardiomyopathy?
p-value: p=<0.05
Deletion of IL-6 mitigates myocardial fibrosis and improves cardiac function in diabetic mice, highlighting IL-6 suppression as a potential therapeutic strategy for diabetic cardiomyopathy.
IL-6 suppression may mitigate diabetic cardiomyopathy; hypothesis-generating and should not change practice.
Interleukin 6 (IL-6) has been shown to be an important regulator of cardiac interstitial fibrosis. In this study, we explored the role of interleukin-6 in the development of diabetic cardiomyopathy and the underlying mechanisms. Cardiac function of IL-6 knockout mice was significantly improved and interstitial fibrosis was apparently alleviated in comparison with wildtype (WT) diabetic mice induced by streptozotocin (STZ). Treatment with IL-6 significantly promoted the proliferation and collagen production of cultured cardiac fibroblasts (CFs). High glucose treatment increased collagen production, which were mitigated in CFs from IL-6 KO mice. Moreover, IL-6 knockout alleviated the up-regulation of TGFβ1 in diabetic hearts of mice and cultured CFs treated with high glucose or IL-6. Furthermore, the expression of miR-29 reduced upon IL-6 treatment, while increased in IL-6 KO hearts. Overexpression of miR-29 blocked the pro-fibrotic effects of IL-6 on cultured CFs. In summary, deletion of IL-6 is able to mitigate myocardial fibrosis and improve cardiac function of diabetic mice. The mechanism involves the regulation of IL-6 on TGFβ1 and miR-29 pathway. This study indicates the therapeutic potential of IL-6 suppression on diabetic cardiomyopathy disease associated with fibrosis.
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Zhang et al. (2016) studied Diabetic cardiomyopathy (n=32). IL-6 knockout vs. Wild-type diabetic mice was evaluated on Cardiac function (EF, FS, E/A ratio) and interstitial fibrosis (p=<0.05). Deletion of IL-6 significantly improved cardiac function and alleviated interstitial fibrosis in streptozotocin-induced diabetic mice compared to wild-type diabetic mice.
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