At least half of heart failure patients do not exhibit a major deficit in cardiac contractility; instead, they present with cardiac stiffness and impaired relaxation. The incidence of such preserved ejection fraction heart failure (HFpEF) sharply increases with age, and is currently the leading cause of hospitalization in the elderly. Thus far, there are limited therapeutic options for HFpEF and improving patient survival remains challenging.

To this end, emerging preclinical evidence suggests a link between HFpEF and dysfunctional cellular quality control mechanisms, such as autophagy. Therefore, we devised this project to investigate how disturbances in autophagy-dependent turnover of cardiac proteins and organelles, including mitochondria, contribute to the pathogenesis of HFpEF, and whether they can be targeted for HFpEF therapy. Eventually, the knowledge gained will help us identify suitable therapeutics and examine their potential effects in experimental models of HFpEF. This hypothesis-driven approach might have major clinical implications for millions of patients with HFpEF worldwide.

ResearchGate

Project funding

Funding EUR 659.940,-