Correction to: Targeting senescent retinal pigment epithelial cells facilitates retinal regeneration in mouse models of age-related macular degeneration

Abstract

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The potential for senotherapy as a novel approach to extend life quality in veterinary medicine

“…In vivo , The senotherapeutic nutlin-3a has been investigated as a treatment for age-related macular degeneration ( 144 ). Treatment of a mouse model with nutlin-3a showed a significant recovery of visual function ( 144 ) and ameliorated retinal degeneration ( 154 ).…”

Nutlin-3a for age-related macular degeneration

“…The phenotypes observed during RPE cellular senescence overlapped with important pathological features of retinas from patients with dry AMD, such as increases in subretinal deposits, alterations in fundus autofluorescence, and thickening of Bruch’s membrane. Taken together, these findings indicate that senescence in the RPE can contribute to retinal degeneration [ 6 ].…”

“…In this regard, we hypothesized that cellular senescence in the RPE might represent a new therapeutic target for AMD. We created a chemical-induced mouse model that exhibited general features of cellular senescence in the RPE, including increases in SA-β-gal, p53, p21, and p16 expression; relocalization of HMGB1; and triggering of the SASP [ 6 ]. In addition, we performed single-cell RNA sequencing–based transcriptome analysis on control and senescent RPE tissues, which revealed increased senescence-associated gene expression and negative regulation of apoptosis, and on a specific cell population [Lee et al, Communications biology, in press].…”

“…We made an effort and were successful in developing a method to counter the senescent RPE for AMD treatment ( Figure 1 ). We utilized a senolytic drug that selectively induces apoptosis in senescent RPE cells by targeting proteins associated with antiapoptotic pathways [ 6 ]. Based on our observation of greater p53 levels in senescent RPE cells than in nonsenescent cells, we hypothesized that an MDM2 antagonist would disrupt the MDM2/p53 protein interaction, increase p53 activity, and trigger p53-dependent apoptosis in senescent cells.…”