| Literature DB >> 25398984 |
Yasuhiro Maejima1, Yun Chen2, Mitsuaki Isobe3, Åsa B Gustafsson4, Richard N Kitsis2, Junichi Sadoshima5.
Abstract
Dysregulation of autophagy, an evolutionarily conserved process for degradation of long-lived proteins and organelles, 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.Entities:
Keywords: autophagy; autosis; mitophagy; protein quality control
Mesh:
Year: 2014 PMID: 25398984 PMCID: PMC4329480 DOI: 10.1152/ajpheart.00711.2014
Source DB: PubMed Journal: Am J Physiol Heart Circ Physiol ISSN: 0363-6135 Impact factor: 4.733