Therapeutic approaches to diabetic cardiomyopathy: Targeting the antioxidant pathway

Michael Arad, Maayan Waldman, Nader G. Abraham, Edith Hochhauser

Research output: Contribution to journalReview articlepeer-review

Abstract

The global epidemic of cardiovascular disease continues unabated and remains the leading cause of death both in the US and worldwide. We hereby summarize the available therapies for diabetes and cardiovascular disease in diabetics. Clearly, the current approaches to diabetic heart disease often target the manifestations and certain mediators but not the specific pathways leading to myocardial injury, remodeling and dysfunction. Better understanding of the molecular events determining the evolution of diabetic cardiomyopathy will provide insight into the development of specific and targeted therapies. Recent studies largely increased our understanding of the role of enhanced inflammatory response, ROS production, as well as the contribution of Cyp-P450-epoxygenase-derived epoxyeicosatrienoic acid (EET), Peroxisome Proliferator-Activated Receptor Gamma Coactivator-1α (PGC-1α), Heme Oxygenase (HO)-1 and 20-HETE in pathophysiology and therapy of cardiovascular disease. PGC-1α increases production of the HO-1 which has a major role in protecting the heart against oxidative stress, microcirculation and mitochondrial dysfunction. This review describes the potential drugs and their downstream targets, PGC-1α and HO-1, as major loci for developing therapeutic approaches beside diet and lifestyle modification for the treatment and prevention of heart disease associated with obesity and diabetes.

Original languageEnglish
Article number106454
JournalProstaglandins and Other Lipid Mediators
Volume150
DOIs
StatePublished - Oct 2020

Keywords

  • Diabetes
  • EET
  • Inflammation
  • Mitochondria
  • Obesity
  • Oxygen radicals
  • PGC1α

Fingerprint

Dive into the research topics of 'Therapeutic approaches to diabetic cardiomyopathy: Targeting the antioxidant pathway'. Together they form a unique fingerprint.

Cite this