Ablation of the stress protease OMA1 protects against heart failure in mice

Rebeca, Acin-Perez, Ana Victoria, Lechuga-Vieco, Maria, del Mar Muñoz, Rocío, Nieto-Arellano, Carlos, Torroja, Fátima, Sánchez-Cabo, Concepción, Jiménez, Andrés, González-Guerra, Isabel, Carrascoso, Cristiane, Benincá, Pedro M., Quiros, Carlos, López-Otín, José María, Castellano, Jesús, Ruíz-Cabello, Luis Jesús, Jiménez-Borreguero, José Antonio, Enríquez

Science Translational Medicine |

Current therapies for heart failure vary depending on the root cause and stage of the disease. Acin-Perez et al . studied the molecular link between mitochondrial dysfunction and heart failure, focusing on OMA1, a protease involved in mitochondrial inner membrane remodeling and cytochrome c release. Using three mouse models of heart failure, they found that cardiomyocytes were protected from mitochondrial reactive oxygen species–induced cell death when OMA1 was ablated. OMA1 could be a therapeutic target for heart failure.

http://stm.sciencemag.org/lookup/doi/10.1126/scitranslmed.aan4935