title: Molecular mechanisms mediating mitochondrial dynamics and mitophagy and their functional roles in the cardiovascular system.
abstract: Mitochondria are essential organelles that produce the cellular energy source, ATP. Dysfunctional mitochondria are involved in the pathophysiology of heart disease, which is associated with reduced levels of ATP and excessive production of reactive oxygen species. Mitochondria are dynamic organelles that change their morphology through fission and fusion in order to maintain their function. Fusion connects neighboring depolarized mitochondria and mixes their contents to maintain membrane potential. In contrast, fission segregates damaged mitochondria from intact ones, where the damaged part of mitochondria is subjected to mitophagy whereas the intact part to fusion. It is generally believed that mitochondrial fusion is beneficial for the heart, especially under stress conditions, because it consolidates the mitochondria's ability to supply energy. However, both excessive fusion and insufficient fission disrupt the mitochondrial quality control mechanism and potentiate cell death. In this review, we discuss the role of mitochondrial dynamics and mitophagy in the heart and the cardiomyocytes therein, with a focus on their roles in cardiovascular disease. This article is part of a Special Issue entitled "Mitochondria: From Basic Mitochondrial Biology to Cardiovascular Disease".
authors.affiliation: Department of Cell Biology & Molecular Medicine, NJ Medical School, Rutgers University, USA; Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Science, Kagoshima University, Japan.
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Ikeda
authors.affiliation: Department of Cell Biology & Molecular Medicine, NJ Medical School, Rutgers University, USA.
authors.forename: Akihiro
authors.initials: A
authors.lastname: Shirakabe
authors.affiliation: Department of Cell Biology & Molecular Medicine, NJ Medical School, Rutgers University, USA.
authors.forename: Christopher
authors.initials: C
authors.lastname: Brady
authors.affiliation: Department of Cell Biology & Molecular Medicine, NJ Medical School, Rutgers University, USA.
authors.forename: Daniela
authors.initials: D
authors.lastname: Zablocki
authors.affiliation: Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Science, Kagoshima University, Japan.
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Ohishi
authors.affiliation: Department of Cell Biology & Molecular Medicine, NJ Medical School, Rutgers University, USA. Electronic address: sadoshju@njms.rutgers.edu.
authors.forename: Junichi
authors.initials: J
authors.lastname: Sadoshima
mesh_terms: D000818:Animals; D001343:Autophagy; D002318:Cardiovascular Diseases / Q000209:etiology; D002320:Cardiovascular Physiological Phenomena; D006801:Humans; D008928:Mitochondria / Q000502:physiology*; D063154:Mitochondrial Dynamics; D063306:Mitophagy
keywords: Drp1; Fission; Fusion; Mitochondria; Mitophagy