Imbalance in energy metabolism is a common feature of chronic metabolic diseases such as diabetes, atherosclerosis, neurodegenerative disorders, and non-alcoholic fatty liver disease, with mitochondrial dysfunction recognized as one of the core mechanisms. Abnormal mitochondrial function leads to oxidative stress, metabolic disturbances, and exacerbated inflammation, thereby driving disease progression. This review systematically explores the specific mechanisms of mitochondrial dysfunction in chronic metabolic diseases and summarizes potential mitochondria-targeted therapeutic strategies. By screening and analyzing relevant literature on mitochondrial dysfunction and chronic metabolic diseases, this study focuses on mitochondrial structure, functional regulation, and pathological mechanisms in disease contexts. Mitochondrial dysfunction manifests distinct mechanisms across different diseases: excessive reactive oxygen species production and calcium homeostasis imbalance in diabetes contribute to microvascular complications, while impaired mitophagy in atherosclerosis aggravates endothelial injury. Additionally, aberrant mitochondrial dynamics significantly promote metabolic dysregulation in obesity and fatty liver disease. Therapeutic strategies targeting mitochondrial dysfunction, such as antioxidant therapy, mitophagy modulation, and emerging mitochondrial transplantation techniques, show promise but require further clinical validation. Future research should emphasize precision mitochondrial interventions and synergistic multi-mechanism therapies to provide novel insights for managing chronic metabolic diseases.

能量代谢失衡是糖尿病、动脉粥样硬化、神经退行性疾病、非酒精性脂肪肝等慢性代谢性疾病的共同特征，而线粒体功能受损被认为是其核心机制之一。线粒体功能障碍会导致氧化应激、代谢紊乱及炎症加剧，进而推动疾病进展。本综述系统探讨线粒体功能障碍在慢性代谢性疾病中的具体作用机制，并总结靶向线粒体的潜在治疗策略。通过检索筛选与线粒体功能障碍及慢性代谢性疾病相关的研究文献，重点分析线粒体结构、功能调控及其在疾病中的病理机制。线粒体功能障碍在不同疾病中表现出异常机制：糖尿病中活性氧过量生成与钙稳态失衡导致微血管病变；动脉粥样硬化中线粒体自噬受损加剧内皮损伤。此外，肥胖症和脂肪肝疾病中线粒体动力学异常显著促进代谢紊乱。靶向线粒体功能障碍的治疗策略（如抗氧化治疗、线粒体自噬调控及新兴的线粒体移植技术）展现出潜力，但仍需进一步临床验证。未来研究应关注线粒体精准干预与多机制协同治疗，为慢性代谢性疾病提供新思路。