Mitochondria are known to play crucial roles in normal cellular physiology and in more recent
years they have been implicated in a wide range of pathologies. Central to both these roles is their
ability to alter their shape interchangeably between two different morphologies: an elongated interconnected
network and a fragmented discrete phenotype - processes which are under the regulation of the
mitochondrial fusion and fission proteins, respectively. In this review article, we focus on the mitochondrial
fusion protein optic atrophy protein 1 (OPA1) in cardiovascular health and disease and we
explore its role as a potential therapeutic target for treating cardiovascular and metabolic disease.
Keywords: Cardiovascular disease, fission, fusion, mitochondrial morphology, OPA1.
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