Linking Mitochondrial Gene Dysregulation to Immune Cell Shifts in Retinitis Pigmentosa.

ABSTRACT: Retinitis pigmentosa (RP) is a hereditary retinal disease characterized by the progressive degeneration of photoreceptor and retinal pigment epithelial (RPE) cells, ultimately leading to significant vision loss. While the pathogenesis of RP is associated with mitochondrial dysfunction and immune-inflammatory responses, the specific interplay between disrupted mitochondrial gene expression and immune cell infiltration remains inadequately understood. While gene therapy has been approved for a subset of RP patients with monogenic mutations such as RPE65-associated RP, it has notable limitations beyond high costs: it only targets single-gene defects and fails to reverse advanced retinal degeneration that has already damaged photoreceptors. Thus, a robust understanding of these relationships c

SUBMITTER: Liang J 

PROVIDER: S-EPMC12644131 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature