About this Research Topic
This Research Topic is part of the Diabetes and Heart Failure series (Volume I).
Type 2 diabetes mellitus (T2DM) and Heart Failure (HF) are two complex multifactorial 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 patients. Several complex pathological mechanisms such as altered oxidative stress, hyperglycemia-induced cellular damage, insulin-resistance and mitochondrial dysfunction are implicated.
In this Research Topic we try to bring the two major diseases together by focusing on common molecular pathways and mechanisms, electrical/mechanical/structural alterations and subsequently on clinical outcomes. We encourage investigators to submit original (basic, translational, and clinical) research articles, clinical trials and reviews to this RT 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. gene-therapy) are welcome.
Of note, studies involving high-throughput “omics” (i.e., metabolomics, transcriptomics, proteomics) and cardiac gene regulation (i.e. epigenetics and non-coding RNAs) may provide insightful elucidations of HF- and diabetes-related biological signals as well as clarify common and specific mechanisms.
Type 2 diabetes mellitus (T2DM) and Heart Failure (HF) are two complex multifactorial 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 patients. Several complex pathological mechanisms such as altered oxidative stress, hyperglycemia-induced cellular damage, insulin-resistance and mitochondrial dysfunction are implicated.
In this Research Topic we try to bring the two major diseases together by focusing on common molecular pathways and mechanisms, electrical/mechanical/structural alterations and subsequently on clinical outcomes. We encourage investigators to submit original (basic, translational, and clinical) research articles, clinical trials and reviews to this RT 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. gene-therapy) are welcome.
Of note, studies involving high-throughput “omics” (i.e., metabolomics, transcriptomics, proteomics) and cardiac gene regulation (i.e. epigenetics and non-coding RNAs) may provide insightful elucidations of HF- and diabetes-related biological signals as well as clarify common and specific mechanisms.
Keywords: heart failure, diabetes, basic research, translational research, clinical outcomes, cellular and molecular pathways, drug discovery, genetic therapy, interventional therapies, omics, gene-regulation, epigenetics, non-coding-RNA
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
