Recent progress in research on molecular mechanisms of autophagy in the heart

Yasuhiro Maejima, Yun Chen, Mitsuaki Isobe, Åsa B. Gustafsson, Richard N. Kitsis, Junichi Sadoshima

Research output: Contribution to journalArticlepeer-review


Dysregulation of autophagy, an evolutionarily conserved process for degradation of long-lived proteins and organ-elles, has been implicated in the pathogenesis of human disease. Recent research has uncovered pathways that control autophagy in the heart and molecular mechanisms by which alterations in this process affect cardiac structure and function. Although initially thought to be a nonselective degradation process, autophagy, as it has become increasingly clear, can exhibit specificity in the degradation of molecules and organelles, such as mitochondria. Furthermore, it has been shown that autophagy is involved in a wide variety of previously unrecognized cellular functions, such as cell death and metabolism. A growing body of evidence suggests that deviation from appropriate levels of autophagy causes cellular dysfunction and death, which in turn leads to heart disease. Here, we review recent advances in understanding the role of autophagy in heart disease, highlight unsolved issues, and discuss the therapeutic potential of modulating autophagy in heart disease.

Original languageEnglish (US)
Pages (from-to)H259-H268
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number4
StatePublished - 2015


  • Autophagy
  • Autosis
  • Mitophagy
  • Protein quality control

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine


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