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An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
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Published on: May 4, 2021

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Targeting GSK-3β for adipose dysfunction and cardiovascular complications of metabolic disease: An entangled

Nasser Alotaiq1, Ahmed S Khalifa2, Amr Youssef2

  • 1Health Sciences Research Center, Imam Muhammad Ibn Saud Islamic University (IMISIU), Riyadh, Kingdom of Saudi Arabia.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|December 27, 2024
PubMed

Insights

Metabolic syndrome links visceral fat dysfunction to cardiovascular disease. Altered Wnt signaling and GSK-3β activity may connect these issues, offering potential therapeutic targets.

Area of Science:

  • Biomedical Science
  • Metabolic Disorders
  • Cardiovascular Research

Background:

  • Metabolic syndrome elevates cardiovascular disease risk, linked to visceral adipose tissue (VAT) dysfunction.
  • VAT dysfunction in metabolic syndrome involves adipocyte hypertrophy, reduced vascularization, and hypoxia, creating a pro-oxidative, pro-inflammatory state.
  • The wingless-type mammary tumor virus integration site family (Wnt) signaling pathway regulates adipose tissue homeostasis.

Purpose of the Study:

  • To investigate the role of Wnt signaling and Glycogen Synthase Kinase-3β (GSK-3β) in linking adipose tissue dysfunction to cardiovascular complications in metabolic syndrome.
  • To explore potential context-specific interventions targeting Wnt signaling and GSK-3β for disease modification.

Main Methods:

  • Review and analysis of existing literature on Wnt signaling, GSK-3β, adipose tissue dysfunction, and cardiovascular disease in metabolic syndrome.
  • Exploration of the mechanistic links between these components.

Main Results:

  • Wnt signaling, particularly through GSK-3β, plays a complex role in obesity, metabolic disorders, and cardiovascular sequelae.
  • Altered Wnt signaling and GSK-3β activity are hypothesized to be a key link between VAT dysfunction and cardiovascular disease development in metabolic syndrome.

Conclusions:

  • Aberrant Wnt signaling and GSK-3β activity represent a potential nexus between adipose tissue dysfunction and cardiovascular complications in metabolic syndrome.
  • Targeting Wnt signaling and GSK-3β may offer novel therapeutic strategies for mitigating cardiovascular risks associated with metabolic syndrome.
Keywords:
Wnt/β‐catenin signalingadipogenesisadipose tissueglycogen synthase kinase‐3βhyperplasiahypertrophy

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