ZFIN ID: ZDB-PUB-140513-147
Developmental processes regulated by the 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) pathway: Highlights from animal studies
Eisa-Beygi, S., Ekker, M., Moon, T.W., Macdonald, R.L., Wen, X.Y.
Date: 2014
Source: Reproductive toxicology (Elmsford, N.Y.)   46C: 115-120 (Review)
Registered Authors: Eisa-Beygi, Shahram, Ekker, Marc
Keywords: Cholesterol, Development, HMGCR, Prenylation, Statins, Teratogenesis, Toxicity
MeSH Terms:
  • Animals
  • Growth/physiology*
  • Hydroxymethylglutaryl CoA Reductases/genetics
  • Hydroxymethylglutaryl CoA Reductases/physiology*
  • Morphogenesis/genetics
  • Neovascularization, Physiologic/genetics
  • Neovascularization, Physiologic/physiology
  • Protein Prenylation/genetics
  • Protein Prenylation/physiology
  • Signal Transduction/physiology
PubMed: 24732207 Full text @ Reprod. Toxicol.
ABSTRACT
The 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) is the rate-limiting enzyme in the biosynthesis of cholesterol and isoprenoids, which are substrates required for post-translational modification of signalling proteins that can potentially regulate various aspects of embryonic development. The HMGCR transcripts are detectable during early embryogenesis in both invertebrates and vertebrates, which suggests a conserved developmental requirement for mevalonate derivatives. Consistently, recent animal and in vitro studies have yielded valuable insights into potential morphogenic parameters that are modulated by HMGCR activity. These developmental end-points include brain and craniofacial morphogenesis, PGC migration and survival, myocardial epithelial migration and fusion, EC migration and survival, and vascular stabilization. By providing a synthesis of these studies, we hope that this review will highlight the need to comprehensively examine the entire suite of developmental processes regulated by HMGCR.
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