Mcl-1-mediated mitochondrial fission protects against stress but impairs cardiac adaptation to exercise

Myeloid cell leukemia-1 (Mcl-1) is a structurally and functionally unique anti-apoptotic Bcl-2 protein. While elevated levels of Mcl-1 contribute to tumor cell survival and drug resistance, loss of Mcl-1 in cardiac myocytes leads to rapid mitochondrial dysfunction and heart failure development. Although Mcl-1 is an anti-apoptotic protein, previous studies indicate that its functions extend beyond regulating apoptosis. Mcl-1 is localized to both the mitochondrial outer membrane and matrix. Here, we have identified that Mcl-1 in the outer mitochondrial membrane mediates mitochondrial fission, which is independent of its anti-apoptotic function.

Source: Journal of Molecular and Cellular Cardiology - July 24, 2020 Category: Cytology Authors: Alexandra G. Moyzis, Navraj S. Lally, Wenjing Liang, Leonardo J. Leon, Rita H. Najor, Amabel M. Orogo, Åsa B. Gustafsson Source Type: research