The transforming growth factor-beta/bone morphogenetic protein signalling pathway in adipogenesis

Int J Biochem Cell Biol. 2012 Mar;44(3):475-9. doi: 10.1016/j.biocel.2011.12.014. Epub 2011 Dec 31.

Abstract

Rising obesity epidemic makes the better understanding of transcription factor networks regulating adipogenesis very challenging. Adipogenesis begins with the commitment of pluripotent mesenchymal stem cells to the adipocyte lineage, followed by terminal differentiation of preadipocytes to mature adipocytes. Among the molecules that influence the decision of progenitor cells to become adipocytes are members of transforming growth factor-beta superfamily and particularly bone morphogenetic proteins. Transforming growth factor-beta and bone morphogenetic proteins exert their biological functions mainly through their downstream molecules, the Smads. Here, we review the role(s) of transforming growth factor-beta/bone morphogenetic protein signalling pathway in adipocyte differentiation. Unravelling the precise mechanism of each molecule/pathway is necessary for developing suitable inhibitors or mimetic agents in order to treat obesity and improve insulin resistance. Current research efforts aim at discovering drugs that reduce fat mass or change the phenotype of adipose tissue into a more thermogenic one.

Publication types

  • Review

MeSH terms

  • Adipogenesis*
  • Animals
  • Anti-Obesity Agents / therapeutic use
  • Biomimetics
  • Bone Morphogenetic Proteins / genetics
  • Bone Morphogenetic Proteins / metabolism*
  • Cell Differentiation
  • Drug Discovery
  • Humans
  • Mesenchymal Stem Cells / metabolism
  • Obesity / drug therapy
  • Obesity / pathology
  • Obesity / physiopathology*
  • Signal Transduction
  • Smad Proteins / metabolism
  • Transcriptional Activation
  • Transforming Growth Factor beta / genetics
  • Transforming Growth Factor beta / metabolism*

Substances

  • Anti-Obesity Agents
  • Bone Morphogenetic Proteins
  • Smad Proteins
  • Transforming Growth Factor beta