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A novel function of CREG in metabolic disorders

Yang Li1, Xiaoxiang Tian1, Quanyu Zhang1

  • 1Cardiovascular Research Institute and Department of Cardiology, General Hospital of Northern Theater Command, Shenyang 110016, Liaoning, China.

Medical Review (2021)
|September 19, 2023
PubMed

Insights

Cellular repressor of E1A-stimulated genes (CREG) is crucial for maintaining cell homeostasis and is increasingly linked to metabolic disorders. This review explores CREG

Area of Science:

  • Biochemistry and Molecular Biology
  • Metabolic Research
  • Cellular Biology

Background:

  • Metabolic disorders represent a significant global health challenge, necessitating novel therapeutic interventions.
  • Cellular repressor of E1A-stimulated genes (CREG) is widely expressed in mammalian tissues and vital for cellular and tissue homeostasis.
  • Emerging evidence highlights CREG's significant role as a mediator in the pathogenesis of metabolic disorders.

Purpose of the Study:

  • To review the structure and molecular regulation of CREG.
  • To discuss CREG's involvement in metabolic disorders.
  • To explore therapeutic strategies targeting CREG for metabolic disorder treatment.

Main Methods:

  • Literature review of studies on CREG structure and function.
  • Analysis of research linking CREG to metabolic disease pathways.
  • Synthesis of current therapeutic approaches targeting CREG.

Main Results:

  • CREG's structure and complex molecular regulatory mechanisms are detailed.
  • CREG's critical role in the development and progression of various metabolic disorders is established.
  • Potential therapeutic strategies involving CREG modulation are identified.

Conclusions:

  • CREG is a key player in maintaining metabolic homeostasis.
  • Targeting CREG presents a promising avenue for developing new treatments for metabolic disorders.
  • Further research into CREG regulation and therapeutic applications is warranted.
Keywords:
CREGNAFLDinsulin resistancemetabolic disordersobesityskeletal muscle energy metabolism

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