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Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
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The cGAS/STING Pathway: Friend or Foe in Regulating Cardiomyopathy.

Weiyue Wang1, Yuanxu Gao1, Hyun Kyoung Lee2,3

  • 1Institute for AI in Medicine, Faculty of Medicine, Macau University of Science and Technology, Macau 999087, China.

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|June 11, 2025
PubMed
Summary
This summary is machine-generated.

Inflammation in cardiomyopathy involves the cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) pathway. Targeting this pathway offers potential therapeutic strategies for inflammatory heart disease.

Keywords:
DNA damagecGAS/STING pathwaycardiomyopathymitochondria

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Area of Science:

  • Cardiovascular Research
  • Immunology
  • Molecular Biology

Background:

  • Inflammation is a key factor in cardiomyopathy, leading to chronic heart dysfunction.
  • The cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) pathway is increasingly recognized for its role in inflammatory responses.
  • The precise mechanisms of cGAS/STING signaling in cardiomyopathy remain unclear.

Purpose of the Study:

  • To review the role of cGAS/STING signaling in various cardiomyopathies.
  • To explore modulation of the cGAS/STING pathway in cardiac disease.
  • To identify therapeutic targets for cGAS/STING-driven inflammation in cardiomyopathy.

Main Methods:

  • Systematic literature review of in vivo, in vitro, and clinical studies.
  • Analysis of agonists and antagonists for cGAS/STING pathway modulation.
  • Integration of human single-cell RNA sequencing (scRNA-seq) data.

Main Results:

  • cGAS/STING pathway activation is implicated in cardiomyopathy-associated inflammation.
  • Specific molecular interventions targeting cGAS/STING have been identified.
  • Potential therapeutic targets for mitigating cGAS/STING-driven inflammation were highlighted.

Conclusions:

  • The cGAS/STING pathway represents a significant therapeutic target for inflammatory cardiomyopathy.
  • Further research is needed to translate these findings into clinical practice.
  • Targeting cGAS/STING may improve outcomes for patients with inflammatory cardiomyopathy.