Mitochondrial dynamics and their role in the pathogenesis of age-related macular degeneration: A comprehensive review

Apr 5, 2026Redox biology

How Changes in Energy-Producing Cell Parts May Contribute to Age-Related Macular Degeneration

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Abstract

Mitochondrial dysfunction is a central pathogenic mechanism in age-related macular degeneration (AMD).

AMD is associated with advanced age, genetic susceptibility, and environmental risk factors.
Dysregulation of mitochondrial processes such as fission, fusion, and biogenesis occurs in AMD.
This dysregulation leads to a fragmented mitochondrial network and bioenergetic deficits.
Excessive oxidative stress and inflammatory responses are linked to mitochondrial dysfunction in AMD.
Structural abnormalities and mitochondrial DNA damage have been observed in experimental models and human tissues.
Therapeutic strategies targeting mitochondrial pathways may offer promising interventions for AMD.

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Age-related macular degeneration (AMD) is a leading cause of irreversible blindness in the elderly and has a multifactorial etiology involving advanced age, genetic susceptibility, and environmental risk factors. Accumulating evidence suggests that mitochondrial dysfunction is a central pathogenic mechanism in AMD, particularly in the retinal pigment epithelium (RPE). The RPE is critical for retinal homeostasis, and its high metabolic activity renders it vulnerable to age-related mitochondrial dysfunction. In AMD, the core processes of mitochondrial dynamics-fission, fusion, biogenesis, and mitophagy-are profoundly dysregulated, leading to a fragmented and dysfunctional mitochondrial network. This failure of quality control results in bioenergetic deficits, excessive oxidative stress, and the release of damage-associated molecular patterns that fuel chronic inflammation and complement-mediated damage. Experimental models and human tissue studies have strengthened the link between mitochondrial dysfunction and AMD pathology, revealing structural abnormalities, mitochondrial DNA (mtDNA) damage, and altered metabolic signatures. Therapeutic strategies targeting mitochondrial pathways, including mitochondria-targeted antioxidants, dynamic modulators, and enhancers of biogenesis and mitophagy, such as agents that restore defective mitophagosome formation, represent promising avenues for intervention. As the field advances, the integration of biomarker development and personalized approaches holds the potential to transform the clinical landscape of AMD by addressing the root causes of cellular dysfunction.

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Mitochondrial dynamics and their role in the pathogenesis of age-related macular degeneration: A comprehensive review

Abstract

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