Epilepsy is a heterogeneous disease with a very complex etiological mechanism, characterized by recurrent and unpredictable abnormal neuronal discharge. Epilepsy patients mainly rely on oral antiseizure medication (ASMs) the for treatment and control of disease progression. However, about 30% patients are resistance to ASMs, leading to the inability to alleviate and cure seizures, which gradually evolve into refractory epilepsy. The most common type of intractable epilepsy is temporal lobe epilepsy. Therefore, in-depth exploration of the causes and molecular mechanisms of seizures is the key to find new methods for treating refractory epilepsy. Mitochondria are important organelles within cells, providing abundant energy to neurons and continuously driving their activity. Neurons rely on mitochondria for complex neurotransmitter transmission, synaptic plasticity processes, and the establishment of membrane excitability. The process by which the autophagy system degrades and metabolizes damaged mitochondria through lysosomes is called mitophagy. Mitophagy is a specific autophagic pathway that maintains cellular structure and function. Mitochondrial dysfunction can produce harmful reactive oxygen species, damage cell proteins and DNA, or trigger programmed cell death. Mitophagy helps maintain mitochondrial quality control and quantity regulation in various cell types, and is closely related to the occurrence and development of epilepsy. The imbalance of mitophagy regulation is one of the causes of abnormal neuronal discharge and epileptic seizures. Understanding its related mechanisms is crucial for the treatment and control of the progression of epilepsy in patients.
Age-related macular degeneration (AMD) is one of the leading causes of vision impairment and blindness in the elderly worldwide, with its prevalence increasing significantly with age. The pathogenesis of AMD is multifactorial, involving genetic predisposition, environmental risk factors, chronic inflammation, and mitochondrial dysfunction. In recent years, mitophagy has emerged as a critical mechanism for maintaining mitochondrial quality control, energy homeostasis, and cellular integrity in retinal pigment epithelium (RPE) and photoreceptor cells. Dysregulated mitophagy leads to the accumulation of damaged mitochondria, excessive reactive oxygen species, and metabolic imbalance, thereby triggering RPE dysfunction, inflammatory amplification, and choroidal neovascularization, which drive AMD progression. Both classical pathways (e.g., PINK1/Parkin) and non-classical pathways (e.g., BNIP3, FUNDC1) have been implicated in AMD pathophysiology. Molecules such as Parkin and p62, as well as multimodal imaging features, hold promise as early biomarkers for disease monitoring. Preclinical studies have shown that small-molecule activators (e.g., Urolithin A, Spermidine) and mitochondria-targeted antioxidants (e.g., MitoQ, SkQ1) can restore mitophagy and alleviate RPE damage. However, current evidence remains limited, as large-scale, long-term clinical trials are lacking. Challenges in drug delivery efficiency, safety, patient stratification, and clinical monitoring tools still hinder translation into practice. Future research should focus on biomarker-driven precision interventions, multicenter randomized controlled trials, and individualized therapeutic strategies. Overall, mitophagy research is transitioning from mechanistic exploration to clinical translation, with promising potential to enable early diagnosis, disease stratification, and precision management of AMD.