Epigenetic regulation in the acute kidney injury to chronic kidney disease transition


Por: Rodríguez-Romo R., Berman N., Gómez A., Bobadilla N.A.

Publicada: 1 oct 2015
Categoría: Nephrology

Resumen:
Epigenetic modifications have emerged as a new, important contributor to gene expression regulation in both normal and pathophysiological conditions. Epigenetics have been studied in many diseases and conditions such as acute kidney injury (AKI), a syndrome with a high prevalence that carries a poor prognosis with increased morbidity and mortality. In addition, it has recently been shown that AKI increases the risk for the development of chronic kidney disease (CKD). The specific molecular mechanisms by which AKI increases the risk of CKD and end stage renal disease (ESRD) remain unknown, although there is new evidence supporting a role of epigenetic changes. The most studied epigenetic regulations in AKI are chromatin compaction, DNA methylation, and histone acetylation/deacetylation. These modifications predominantly increase the production of pro-inflammatory and profibrotic cytokines such as: monocyte chemoattractant protein-1 (MCP-1), complement protein 3 (C3), transforming growth factor ß (TGF-ß) that have been shown for perpetuating inflammation, promoting epithelial-to-mesenchymal transition (EMT) and ultimately causing renal fibrosis. A review of epigenetic mechanisms, the pathophysiology of AKI and recent studies that implicate epigenetic modifications in AKI and in the transition to CKD are discussed below. © 2015 Asian Pacific Society of Nephrology.

Filiaciones:
Rodríguez-Romo R.:
 Univ Nacl Autonoma Mexico, Inst Invest Biomed, Mol Physiol Unit, Mexico City 04510, DF, Mexico

Berman N.:
 Univ Nacl Autonoma Mexico, Inst Invest Biomed, Mol Physiol Unit, Mexico City 04510, DF, Mexico

Gómez A.:
 Univ Nacl Autonoma Mexico, Inst Invest Biomed, Mol Physiol Unit, Mexico City 04510, DF, Mexico

Bobadilla N.A.:
 Univ Nacl Autonoma Mexico, Inst Invest Biomed, Mol Physiol Unit, Mexico City 04510, DF, Mexico
ISSN: 13205358
Editorial
WILEY-BLACKWELL, 111 RIVER ST, HOBOKEN 07030-5774, NJ USA, Estados Unidos America
Tipo de documento: Review
Volumen: 20 Número: 10
Páginas: 736-743
WOS Id: 000361466700009
ID de PubMed: 26015167
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