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Review
. 2024 May 23:19:939-951.
doi: 10.2147/CIA.S463297. eCollection 2024.

Age-Related Macular Degeneration: A Disease of Cellular Senescence and Dysregulated Immune Homeostasis

Affiliations
Review

Age-Related Macular Degeneration: A Disease of Cellular Senescence and Dysregulated Immune Homeostasis

Cunzi Li et al. Clin Interv Aging. .

Abstract

Age-related macular degeneration (AMD) is a degenerative ocular disease primarily affecting central vision in the elderly. Its pathogenesis is complex, involving cellular senescence and immune homeostasis dysregulation. This review investigates the interaction between these two critical biological processes in AMD pathogenesis and their impact on disease progression. Initially, cellular senescence is analyzed, with particular emphasis on retinal damage induced by senescent retinal pigment epithelial cells. Subsequently, the occurrence of immune homeostasis dysregulation within the retina and its mechanistic role in AMD areis explored. Furthermore, the paper also discusses in detail the interplay between cellular senescence and immune responses, forming a vicious cycle that exacerbates retinal damage and may influence treatment outcomes. In summary, a deeper understanding of the interrelation between cellular senescence and immune dysregulation is vital for the developing innovative therapeutic strategies for AMD.

Keywords: age-related macular degeneration; cellular senescence; immune homeostasis dysregulation.

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Conflict of interest statement

The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
Physiologic and Pathologic Images of the Retina. (a) Structure diagram of retinal layers and immunosuppressive mechanism in the retina; (b) Pathological changes in dry AMD: drusen formation, RPE dysfunction; (c) Pathological changes in wet AMD: CNV formation, photoreceptor/RPE/BM/CC atrophy and dysfunction.
Figure 2
Figure 2
Vicious Cycle. Mechanisms of interaction between cellular senescence and dysregulation of immune homeostasis in retina.

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