Type 2 diabetes mellitus (T2DM) and Heart Failure (HF) are two complex multi factorial diseases that can coexist and strongly amplify each other, suggesting overlapping mechanisms contributing to disease state.
T2DM patients with HF have a higher risk of mortality and hospitalization for HF than no diabetics. Therefore, there is an increasing necessity to find new diagnostic instruments and treatments to improve clinical outcomes in T2DM failing heart subjects.
Several and complex pathological mechanisms such as altered cardiac ionic homeostasis, oxidative stress, hyperglycemia-induced cellular damage and mitochondrial dysfunction are implicated. Importantly, altered cardiac ionic homeostasis is an established signature and driver of HF pathology but has been largely neglected in T2DM pathology. There, insulin resistance and disturbances in glucose and fatty acid metabolism are currently viewed as major instigators of T2DM. However, older and recent researches indicate that cardiac ionic disturbances may actually provide the common ground for both diseases and explain, at least in part, why they mutually amplify each other. Intriguingly, these changes may lead to electrical and mechanical alterations in systolic and diastolic electrical phases.
Therefore, in this Research Topic (RT) we try to bring the two major diseases together by focusing on common molecular pathways and mechanisms, electrical/mechanical alterations and subsequently on clinical outcomes.
We encourage investigators to submit to this RT both original research articles, clinical trials and reviews having the purpose to address novel diagnostic tools or new therapeutic treatments for T2DM and HF. Manuscripts involving therapies with already proven efficacy (e.g. SGLT2 inhibitors) or potential suggested efficacy (e.g. epigenetic therapy) are welcome.
Type 2 diabetes mellitus (T2DM) and Heart Failure (HF) are two complex multi factorial diseases that can coexist and strongly amplify each other, suggesting overlapping mechanisms contributing to disease state.
T2DM patients with HF have a higher risk of mortality and hospitalization for HF than no diabetics. Therefore, there is an increasing necessity to find new diagnostic instruments and treatments to improve clinical outcomes in T2DM failing heart subjects.
Several and complex pathological mechanisms such as altered cardiac ionic homeostasis, oxidative stress, hyperglycemia-induced cellular damage and mitochondrial dysfunction are implicated. Importantly, altered cardiac ionic homeostasis is an established signature and driver of HF pathology but has been largely neglected in T2DM pathology. There, insulin resistance and disturbances in glucose and fatty acid metabolism are currently viewed as major instigators of T2DM. However, older and recent researches indicate that cardiac ionic disturbances may actually provide the common ground for both diseases and explain, at least in part, why they mutually amplify each other. Intriguingly, these changes may lead to electrical and mechanical alterations in systolic and diastolic electrical phases.
Therefore, in this Research Topic (RT) we try to bring the two major diseases together by focusing on common molecular pathways and mechanisms, electrical/mechanical alterations and subsequently on clinical outcomes.
We encourage investigators to submit to this RT both original research articles, clinical trials and reviews having the purpose to address novel diagnostic tools or new therapeutic treatments for T2DM and HF. Manuscripts involving therapies with already proven efficacy (e.g. SGLT2 inhibitors) or potential suggested efficacy (e.g. epigenetic therapy) are welcome.
