The prevalence of metabolic disease and heart failure – collectively named cardiometabolic disease – is rising sharply worldwide. The mechanisms underlying the metabolic disturbances of the two most common forms of heart failure, heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF) remain ill-defined. Epidemiological observations suggest that increased adiposity and increased levels of circulating inflammatory biomarkers are major contributing mechanisms of HF pathogenesis. Indeed, lipotoxicity and chronic low-grade metabolic inflammation, termed “metainflammation,” have been suggested to play a major role in the pathogenesis of myocardial alterations in both HFrEF and HFpEF. However, mechanisms of cardiac lipotoxicity and metainflammation in HF are largely unknown. Through the employment of multiple experimental approaches, including in vivo and in vitro disease-modeling, our group will address these fundamental challenges directly.
Heart failure and metabolic disease – obesity, metabolic syndrome and diabetes – are epidemiologically and pathophysiologically intertwined. Our group is broadly interested in understanding how metabolic alterations contribute to the pathogenesis of the different forms of heart failure.