ReviewAdvances in experimental medicine and biology2025
Mitochondrial DNA Damage in the Retinal Pigmented Epithelium (RPE) and Its Role in RPE Pathobiology.
Review in Advances in experimental medicine and biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Baicalin Protects ARPE-19 Cells Against BRVO-Related Hypoxic Injury by Preserving Mitochondrial Function and Inhibiting Ferroptosis.Antioxidants (Basel, Switzerland) · 2026Article
- Photobiomodulation in Age-Related Macular Degeneration: A Mitochondrial Bioenergetic Framework and Translational Perspective.Life (Basel, Switzerland) · 2026Review
- The key mechanisms and intervention strategies of cell-type-specific mitochondrial metabolism in ophthalmic diseases.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Retinal pigmented epithelial (RPE) cells have critical functions in the retina. These cells rely heavily on their mitochondria to generate energy, offer metabolites for biosynthesis through the TCA cycle, regulate apoptosis, and process lipids from photoreceptors. Therefore, mitochondrial damage has significant consequences for the RPE and, by proxy, photoreceptors. Researchers have identified damaged mitochondrial DNA (mtDNA) accumulation in patient samples from aged and diseased individuals. These damages include point mutations and complete deletions of mtDNA segments. The most significant observation in these studies is a positive correlation between the accumulation of damaged mtDNA with the stage of AMD rather than aging. This chapter will discuss how mitochondrial dysfunction in the RPE can drive disease pathobiology by altering their physiological functions.
Indexed as
Identifiers
39930225What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.