<p>Preservation of skeletal muscle mass and function is a key feature of healthy ageing and relies on the tight coordination between protein synthesis and breakdown to maintain proteostatic balance. These processes impose a substantial energetic demand, highlighting the importance of mitochondrial function in skeletal muscle homeostasis. Increasing evidence indicates that mitochondria and the sarcoplasmic reticulum are functionally interconnected. Effective crosstalk between these organelles contributes to the integration of bioenergetic supply, Ca²⁺ handling, and proteostasis. Disruption of this communication network may impair adaptive stress responses, compromise protein quality control, and favour the development of anabolic resistance during ageing. This review synthesizes current evidence on mitochondria–sarcoplasmic reticulum communication. It further discusses how disruption of this crosstalk may promote anabolic resistance and skeletal muscle atrophy, with particular emphasis on its implications for age-related muscle decline.</p>

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Mitochondria–sarcoplasmic reticulum crosstalk as a modulator of skeletal muscle mass

  • Rafael A. Casuso

摘要

Preservation of skeletal muscle mass and function is a key feature of healthy ageing and relies on the tight coordination between protein synthesis and breakdown to maintain proteostatic balance. These processes impose a substantial energetic demand, highlighting the importance of mitochondrial function in skeletal muscle homeostasis. Increasing evidence indicates that mitochondria and the sarcoplasmic reticulum are functionally interconnected. Effective crosstalk between these organelles contributes to the integration of bioenergetic supply, Ca²⁺ handling, and proteostasis. Disruption of this communication network may impair adaptive stress responses, compromise protein quality control, and favour the development of anabolic resistance during ageing. This review synthesizes current evidence on mitochondria–sarcoplasmic reticulum communication. It further discusses how disruption of this crosstalk may promote anabolic resistance and skeletal muscle atrophy, with particular emphasis on its implications for age-related muscle decline.