Changes in mitochondrial morphology and alterations in mitochondrial energetics contribute to the chronic energy deficit and mechanical dysfunction in heart failure progression.
This review highlights the critical role of mitochondrial dysfunction, including altered morphology and energetics, in the progression of heart failure.
This review focuses on the evidence accumulated in humans and animal models to the effect that mitochondria are key players in the progression of heart failure (HF). Mitochondria are the primary source of energy in the form of adenosine triphosphate that fuels the contractile apparatus, and are thus essential for the pumping activity of the heart. We evaluate changes in mitochondrial morphology and alterations in the main components of mitochondrial energetics, such as substrate utilization and oxidative phosphorylation coupled with the level of respirasomes, in the context of their contribution to the chronic energy deficit and mechanical dysfunction in HF.
Rosca et al. (Wed,) conducted a review in Heart failure. Changes in mitochondrial morphology and alterations in mitochondrial energetics contribute to the chronic energy deficit and mechanical dysfunction in heart failure progression.