Molecular mechanisms mediating mitochondrial dynamics and mitophagy and their functional roles in the cardiovascular system

Yoshiyuki Ikeda, Akihiro Shirakabe, Christopher Brady, Daniela Zablocki, Mitsuru Ohishi, Junichi Sadoshima

Research output: Contribution to journalReview articlepeer-review

99 Scopus citations

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".

Original languageEnglish (US)
Pages (from-to)116-122
Number of pages7
JournalJournal of Molecular and Cellular Cardiology
Volume78
DOIs
StatePublished - Jan 1 2015

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

Keywords

  • Drp1
  • Fission
  • Fusion
  • Mitochondria
  • Mitophagy

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