Hypoxia-induced myocardial regeneration

Wataru Kimura, Yuji Nakada, Hesham A. Sadek

Research output: Contribution to journalReview articlepeer-review

28 Scopus citations


The underlying cause of systolic heart failure is the inability of the adult mammalian heart to regenerate damaged myocardium. In contrast, some vertebrate species and immature mammals are capable of full cardiac regeneration following multiple types of injury through cardiomyocyte proliferation. Little is known about what distinguishes proliferative cardiomyocytes from terminally differentiated, nonproliferative cardiomyocytes. Recently, several reports have suggested that oxygen metabolism and oxidative stress play a pivotal role in regulating the proliferative capacity of mammalian cardiomyocytes. Moreover, reducing oxygen metabolism in the adult mammalian heart can induce cardiomyocyte cell cycle reentry through blunting oxidative damage, which is sufficient for functional improvement following myocardial infarction. Here we concisely summarize recent findings that highlight the role of oxygen metabolism and oxidative stress in cardiomyocyte cell cycle regulation, and discuss future therapeutic approaches targeting oxidative metabolism to induce cardiac regeneration.

Original languageEnglish (US)
Pages (from-to)1676-1681
Number of pages6
JournalJournal of applied physiology
Issue number6
StatePublished - 2017


  • Cardiac regeneration
  • Cardiomyocyte proliferation
  • Hypoxia
  • Oxygen metabolism

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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