Sarcopenia, the loss of muscle mass and strength in aging individuals, is driven by multiple mechanisms, including loss of muscle stem cell activity and dysfunction of neuromuscular junctions. In addition, chronic inflammation and mitochondrial dysfunction also play a significant role in the development of sarcopenia. Mitochondrial dysfunction leads to disturbances in muscle architecture and functionality, while chronic inflammation exacerbates the negative effects of mitochondrial dysfunction. Understanding the interplay between these factors is crucial for developing innovative pharmacotherapies to manage sarcopenia in the elderly population.
This analytical review examines the complex interplay between mitochondrial dysfunction, persistent inflammation, and the pathogenesis of sarcopenia. It emphasizes the need to alleviate inflammation and correct mitochondrial anomalies in geriatric populations to prevent and manage sarcopenia. The review provides a comprehensive overview of the direct correlation between mitochondrial dysfunction and the genesis of sarcopenia, highlighting the potential synergistic effects between inflammatory responses and mitochondrial insufficiencies during the aging of skeletal muscle. This sheds light upon emergent therapeutic objectives in the fight against sarcopenia.
