Modulating autophagy to treat cardiovascular disease
- Luca SCORRANO, University of Padova, (Italy)
- Junichi SADOSHIMA, Rutgers New Jersey Medical School, Newark (USA)
- Ana Maria CUERVO, Richard KITSIS, Albert Einstein College of Medicine of Yeshiva University, Bronx (USA)
- Guido KROEMER, Institut Gustave Roussy, Villejuif (France)
- Michael SHILOH, University of Texas Southwestern Medical Center, Dallas (USA)
- Kinya OTSU, King’s College London (UK)
- Judith SLUIMER, Maastricht University Medical Center (Netherlands)
Autophagy is a process in which cellular proteins, lipids, and organelles are transported to specialized processing centers called lysosomes for degradation. It is becoming clear that autophagy is critical to a number of functions within the cell, including protein and organelle quality control, defense against cellular stresses, and metabolic regulation. Autophagy can also be damaging to cells. It is believed to play a role in ischemia reperfusion injury, a phenomenon where the tissue supplied by an artery that becomes blocked, such as during a heart attack or stroke, is at risk of cell death when the artery becomes unblocked and blood flow is re-established. Network investigators begin from the premise that the heart and blood vessels, continually under metabolic and mechanical stress, are relatively more dependent on autophagy to maintain normal function than other tissues. The Leducq network will study how autophagy functions as a protective or damaging process in the pathogenesis of cardiovascular disease. Potential therapeutics to modulate autophagy, already developed by the team, will be tested in relevant animal models with respect to their abilities to preserve cardiac and vascular function.