PMID- 26015167
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 1440-1797 (Electronic)
IS  - 1320-5358 (Linking)
VI  - 20
IP  - 10
DP  - 2015 Oct
TI  - Epigenetic regulation in the acute kidney injury to chronic kidney disease 
      transition.
PG  - 736-743
LID - 10.1111/nep.12521 [doi]
AB  - 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 beta (TGF-beta) 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.
CI  - (c) 2015 Asian Pacific Society of Nephrology.
FAU - Rodriguez-Romo, Roxana
AU  - Rodriguez-Romo R
AD  - Molecular Physiology Unit, Instituto de Investigaciones Biomedicas, Universidad 
      Nacional Autonoma de Mexico, Mexico City, Mexico.
AD  - Department of Nephrology, Instituto Nacional de Ciencias Medicas y Nutricion 
      Salvador Zubiran, Mexico City, Mexico.
FAU - Berman, Nathan
AU  - Berman N
AD  - Molecular Physiology Unit, Instituto de Investigaciones Biomedicas, Universidad 
      Nacional Autonoma de Mexico, Mexico City, Mexico.
AD  - Department of Nephrology, Instituto Nacional de Ciencias Medicas y Nutricion 
      Salvador Zubiran, Mexico City, Mexico.
FAU - Gomez, Arturo
AU  - Gomez A
AD  - Molecular Physiology Unit, Instituto de Investigaciones Biomedicas, Universidad 
      Nacional Autonoma de Mexico, Mexico City, Mexico.
AD  - Department of Nephrology, Instituto Nacional de Ciencias Medicas y Nutricion 
      Salvador Zubiran, Mexico City, Mexico.
FAU - Bobadilla, Norma A
AU  - Bobadilla NA
AD  - Molecular Physiology Unit, Instituto de Investigaciones Biomedicas, Universidad 
      Nacional Autonoma de Mexico, Mexico City, Mexico.
AD  - Department of Nephrology, Instituto Nacional de Ciencias Medicas y Nutricion 
      Salvador Zubiran, Mexico City, Mexico.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Australia
TA  - Nephrology (Carlton)
JT  - Nephrology (Carlton, Vic.)
JID - 9615568
OTO - NOTNLM
OT  - DNA condensation
OT  - histone acetylation/deacetylation
OT  - histones
OT  - methylation
EDAT- 2015/05/28 06:00
MHDA- 2015/05/28 06:01
CRDT- 2015/05/28 06:00
PHST- 2015/05/20 00:00 [accepted]
PHST- 2015/05/28 06:00 [pubmed]
PHST- 2015/05/28 06:01 [medline]
PHST- 2015/05/28 06:00 [entrez]
AID - 10.1111/nep.12521 [doi]
PST - ppublish
SO  - Nephrology (Carlton). 2015 Oct;20(10):736-743. doi: 10.1111/nep.12521.