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Mitochondrial innate immune signaling in skeletal muscle adaptation to exercise.

Jin Ma¹, Annie Yujin Son¹, Youlim Son¹

¹Cardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892, USA.

Trends in Endocrinology and Metabolism: TEM

|June 13, 2025

View abstract on PubMed

Summary

Exercise-induced inflammation, mediated by the cGAS-STING-NF-κB pathway, promotes metabolic adaptation. Targeting this pathway, involving mitochondrial proteins CHCHD4 and TRIAP1, may offer exercise-like health benefits.

Keywords:

CHCHD4 TRIAP1 exercise fiber type

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Area of Science:

Immunology
Exercise Physiology
Mitochondrial Biology

Background:

Exercise triggers inflammation as a response to muscle damage.
Controlled immune signaling aids metabolic adaptation, combating obesity and diabetes.
Mitochondria are crucial for innate immune signaling beyond oxidative metabolism.

Purpose of the Study:

To review recent findings on the role of the cGAS-STING-NF-κB pathway in exercise adaptation.
To explore the involvement of mitochondrial proteins CHCHD4 and TRIAP1 in this pathway.
To assess the potential of targeting this pathway for health benefits.

Main Methods:

Literature review of recent research on immune signaling in skeletal muscle.
Analysis of the cGAS-STING-NF-κB pathway activation by mitochondrial protein downregulation.

Examination of studies on CHCHD4 haploinsufficiency in mouse models.

Main Results:

The cGAS-STING-NF-κB pathway, activated by CHCHD4 and TRIAP1 downregulation, mediates skeletal muscle adaptation to exercise.
This pathway enhances cellular resilience to environmental stresses.
CHCHD4 deficiency in mice prevented obesity, suggesting a link to metabolic health.

Conclusions:

The cGAS-STING-NF-κB innate immune pathway is a key mediator of exercise-induced skeletal muscle adaptation.
Targeting this pathway, particularly CHCHD4, presents a potential strategy for achieving exercise-related health benefits, including obesity prevention.