The treatments target myocardial fibrosis, inflammation, oxidative stress and insulin resistance.
Several potential treatments for diabetes-associated cardiovascular disease have shown promising results in preclinical animal studies and warrant randomized clinical trials to validate their effectiveness, according to a recent study published in Nature Reviews Cardiology.
The treatments target myocardial fibrosis, inflammation, oxidative stress and insulin resistance. Pathophysiological factors such as metabolic disturbances, insulin resistance, formation and crosslinking of advanced glycation end products, mitochondrial damage, oxidative stress, inflammation, and cell death contribute to diabetic cardiomyopathy.
Diabetic cardiomyopathy typically includes cardiac hypertrophy and fibrosis, early-onset diastolic dysfunction and late-onset systolic dysfunction. Current treatments for diabetes-associated cardiovascular disease focus on optimizing glycemic control, lowering lipid levels and reducing oxidative stress — all conventional therapies.
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“Sensitive and specific markers for changes in intracellular signaling pathways involved in the pathogenesis of diabetic cardiomyopathy, as well as novel cardioprotective strategies targeting these pathways, will hopefully improve cardiovascular outcomes in patients with diabetes,” according to authors of the study, “Mechanisms of Diabetic Cardiomyopathy and Potential Therapeutic Strategies: Preclinical and Clinical Evidence.”
The study’s authors included:
- Yi Tan, Ph.D., assistant professor of pediatrics at the University of Louisville School of Medicine
- Kupper A. Wintergerst, M.D., director of the Wendy Novak Diabetes Institute, endocrinologist with Norton Children’s Endocrinology, affiliated with the UofL School of Medicine, and division chief of pediatric endocrinology.
- Lu Cai, M.D, Ph.D., professor of pediatrics, radiation oncology, and pharmacology and toxicology, and director of the Pediatric Research Institute, Department of Pediatrics, at the UofL School of Medicine.