Enhanced NCLX-dependent mitochondrial Ca2+ efflux attenuates pathological remodeling in heart failure

Mitochondrial calcium (mCa2+) uptake couples changes in cardiomyocyte energetic demand to mitochondrial ATP production. However, excessive mCa2+ uptake triggers permeability transition and necrosis. Despite these established roles during acute stress, the involvement of mCa2+ signaling in cardiac adaptations to chronic stress remains poorly defined. Changes in NCLX expression are reported in heart failure (HF) patients and models of cardiac hypertrophy. Therefore, we hypothesized that altered mCa2+ homeostasis contributes to the hypertrophic remodeling of the myocardium that occurs upon a sustained increase in cardiac workload.

Source: Journal of Molecular and Cellular Cardiology - March 28, 2022 Category: Cytology Authors: Joanne F. Garbincius, Timothy S. Luongo, Pooja Jadiya, Alycia N. Hildebrand, Devin W. Kolmetzky, Adam S. Mangold, Rajika Roy, Jessica Ibetti, Mary Nwokedi, Walter J. Koch, John W. Elrod Source Type: research