Why the study?
Although CCR2 plays an important role in diabetes, its role in diabetic cardiomyopathy had not been examined.
Does CCR2 knockout or inhibition improve cardiac dysfunction and fibrosis in mouse models of diabetic cardiomyopathy?
Does CCR2 knockout or inhibition improve cardiac dysfunction and fibrosis in mouse models of diabetic cardiomyopathy?
CCR2 knockout or pharmacological inhibition improves cardiac dysfunction and fibrosis in mouse models of diabetic cardiomyopathy, identifying CCR2 as a potential novel therapeutic target.
Hypothesis-generating for CCR2 inhibition in diabetic cardiomyopathy; human studies needed before clinical translation.
CCR2 has been proven to play an important role in diabetes. However, the role of CCR2 in diabetic cardiomyopathy has not been examined. In this study, we investigated the effects of cardiac CCR2 on diabetic cardiomyopathy. We created a model of streptozotocin (STZ)–induced diabetic cardiomyopathy. Expression of CCR2 was upregulated in the hearts of STZ-induced diabetic mice. CCR2 knockout significantly improved STZ-induced cardiac dysfunction and fibrosis. Moreover, deletion of CCR2 inhibited STZ-induced apoptosis and the production of STZ-induced reactive oxygen species in the heart. CCR2 knockout resulted in M2 polarization in hearts of STZ-treated mice. Treatment with a CCR2 inhibitor reversed hyperglycemia-induced cardiac dysfunction in db/db mice. These results suggest that CCR2-induced inflammation and oxidative stress in the heart are involved in the development of diabetic cardiomyopathy and that CCR2 could be a novel target for therapy.
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Tan et al. (2019) studied this question.
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