Chronic inflammation driven by hyperglycemia and hyperlipidemia contributes to diabetic cardiomyopathy, highlighting inflammatory signaling pathways as potential therapeutic targets.
This review highlights the critical role of inflammatory signaling in the pathogenesis of diabetic cardiomyopathy and explores potential therapeutic targets to halt disease progression.
Diabetes mellitus and the associated increased risk of cardiovascular disease is a major health-care issue worldwide. Diabetic cardiomyopathy, a complication of diabetes mellitus, is driven primarily by hyperglycaemia and hyperlipidaemia, which promote cardiac oxidative stress, mitochondrial dysfunction and pathological cardiac remodelling, leading to impaired cardiac function and eventual heart failure. Over the past 30 years, research on diabetic cardiomyopathy and other diabetes-associated cardiovascular diseases has focused on the role of chronic inflammation. Inflammation is a complex process involving pro-inflammatory cytokines, chemokines, activation of resident immune cells, and recruitment of immune cells to sites of injury, processes that are exacerbated in the setting of diabetes. Evidence now suggests that the inflammatory processes caused by persistent hyperglycaemia and hyperlipidaemia in diabetes contribute to the impairment of cardiac function. Importantly, no treatment options are available to reverse diabetic cardiomyopathy, with clinicians relying on strategies to delay or halt the progression of the disease. In this Review, we describe the inflammatory signalling pathways involved in diabetic cardiomyopathy and discuss strategies that can potentially be used to target these inflammatory pathways for the treatment of diabetic cardiomyopathy.
Blasio et al. (Fri,) conducted a review in Diabetic cardiomyopathy. Chronic inflammation driven by hyperglycemia and hyperlipidemia contributes to diabetic cardiomyopathy, highlighting inflammatory signaling pathways as potential therapeutic targets.