Mitochondria are highly dynamic and semi-autonomous organelles, essential for many fundamental cellular processes, including energy production, metabolite synthesis, ion homeostasis, lipid metabolism and initiation of apoptotic cell death. Proper mitochondrial physiology is a prerequisite for health and survival. Generation of new and removal of damaged or unwanted mitochondria are tightly controlled processes that need to be accurately coordinated for the maintenance of mitochondrial and cellular homeostasis. Mitophagy is a conserved, mitochondria-specific autophagic clearance process. An intricate regulatory network balances mitophagy with mitochondrial biogenesis. Proper coordination of these opposing processes is important for stress resistance and longevity. Age-dependent decline of mitophagy both inhibits removal of dysfunctional or superfluous mitochondria and impairs mitochondrial biogenesis resulting in progressive mitochondrial accretion and consequently, deterioration of cell function. Nodal regulatory factors that contribute to mitochondrial homeostasis have been implicated in the pathogenesis of several age-associated pathologies, such as neurodegenerative and cardiovascular disorders and cancer, among others. Thus, mitophagy is emerging as a potential target for therapeutic interventions against diseases associated with ageing. In this review, we survey the molecular mechanisms that govern and interface mitophagy with mitochondrial biogenesis, focusing on key elements that hold promise for the development of pharmacological approaches towards enhancing healthspan and quality of life in the elderly.

线粒体是高度动态和半自治的细胞器，对于许多基本细胞过程至关重要，包括能量产生，代谢产物合成，离子稳态，脂质代谢和凋亡细胞死亡的起始。正确的线粒体生理是健康和生存的先决条件。产生新的和清除损坏的或不需要的线粒体是严格控制的过程，需要对其进行精确协调以维持线粒体和细胞体内平衡。线粒体是一种保守的线粒体特异性自噬清除过程。复杂的调节网络在线粒体与线粒体生物发生之间取得平衡。这些对立过程的正确协调对于抵抗压力和延长寿命至关重要。依赖年龄的线粒体下降既抑制功能障碍或多余的线粒体的去除，又损害线粒体的生物发生，导致线粒体进行性积聚，从而导致细胞功能恶化。促成线粒体动态平衡的节点调节因子已牵涉到几种与年龄相关的病理学的发病机理中，例如神经退行性疾病和心血管疾病以及癌症等。因此，线粒体正在成为针对与衰老相关的疾病的治疗性干预的潜在靶标。在这篇综述中，我们调查了控制和吞噬线粒体与线粒体生物发生的分子机制，