Regulation of Cell Death Through the Mitochondria
We are investigating the molecular mechanisms that underlie cell death in general, as well as the potential medical benefits that might arise from inhibition of death in certain disease states. For example, inhibition of cell death in the heart could potentially rescue an individual from death or serious disease following myocardial infarction injury. Moreover, the progressive loss of pump function over time that characterizes heart failure is precipitated, in part, by the gradual loss of cardiac myocytes through programmed cell death. In skeletal muscle, progressive loss of myofibers associated with muscular dystrophy is also regulated by specific molecular pathways that mediate apoptotic and/or necrotic cell death. Thus, inhibition of nodal cell death pathways could have a significant impact in combating diseases of striated muscle. We are currently focusing most of our efforts on elucidating the mitochondrial (intrinsic) cell death pathway, with a specific emphasis on the process of mitochondrial permeability pore formation. We have shown that permeability transition, as regulated by cyclophilin D in the inner mitochondrial matrix, serves a nodal function in controlling cell death in response to oxidative injury and calcium overload. We are extending these and other key observations in an attempt to better characterize the molecular underpinnings of cell death in mammalian tissues.
Contact Us
The Molkentin Laboratory is part of the Division of Molecular Cardiovascular Biology at Cincinnati Children's Research Foundation. The lab is located in Location R (Research Foundation Building), Room 3030.
Jeffery D. Molkentin PhD
Professor
Cincinnati Children's Hospital Medical Center
3333 Burnet Ave, MLC7020
Room 3030
Cincinnati, OH 45229-3039
Telephone: 513-636-3557
Email: jeff.molkentin@cchmc.org
