Update on the pathophysiological activities of the cardiac molecule cardiotrophin-1 in obesity

Mohamed Asrih1, François Mach, Alessandra Quercioli

  • 1Division of Cardiology, Faculty of Medicine, University of Geneva and Geneva University Hospital, Foundation for Medical Researches, Geneva 4, Switzerland.

Insights

Cardiotrophin-1 (CT-1) plays a dual role in obesity, potentially improving metabolism but also causing adverse effects like cardiac hypertrophy. Further research is needed to clarify its therapeutic potential and role in obesity-related cardiovascular diseases.

Area of Science:

  • Endocrinology
  • Cardiovascular Biology
  • Metabolic Research

Background:

  • Cardiotrophin-1 (CT-1) is a cytokine primarily targeting the heart but also affecting liver, adipose tissue, and arteries.
  • CT-1 signals through a receptor complex involving LIFRβ and gp130.
  • Elevated CT-1 levels are linked to obesity and metabolic syndrome, possibly due to adipose tissue overexpression.

Purpose of the Study:

  • To review and update evidence on the pathophysiological roles of CT-1 in obesity.
  • To discuss the potential therapeutic applications of CT-1 in obesity and related conditions.
  • To explore CT-1's role as a damage/danger-associated molecular pattern (DAMP) in obesity-related cardiovascular diseases.

Main Methods:

  • Narrative review of existing basic research.
  • Analysis of studies investigating CT-1 concentrations in obesity and metabolic syndrome.
  • Examination of animal model data on exogenous CT-1 treatment effects.

Main Results:

  • CT-1 concentrations are elevated in obesity and metabolic syndrome.
  • Exogenous CT-1 improves lipid and glucose metabolism in animal models of obesity.
  • CT-1 can induce adverse effects, including cardiac hypertrophy and adipose tissue inflammation.

Conclusions:

  • CT-1 exhibits both beneficial metabolic effects and detrimental impacts in obesity.
  • CT-1's dual nature suggests a complex role in obesity-related pathophysiology.
  • Further investigation is required to establish CT-1's therapeutic potential and its role as a DAMP in cardiovascular disease.

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