Evidence map›Paper›PMID 42774060›Full record

ArticleMolecular vision2026

Assessing mitochondrial phenotypes in a cybrid model of dry age-related macular degeneration.

Jacob Dohl, Nyan Lin Zaw, Jett Nguyen, Gordon Burns, Brandon Park, Shari Atilano, Kevin Schneider, Marilyn Chwa, Maria Cristina Kenney

Abstract read
In one paragraph

Article in Molecular vision, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Jacob DohlDepartment of Pathology and Laboratory Medicine, University of California Irvine, Irvine, CA.
Nyan Lin ZawDepartment of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA.
Jett NguyenDepartment of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA.
Gordon BurnsDepartment of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA.
Brandon ParkDepartment of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA.
Shari AtilanoDepartment of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA.
Kevin SchneiderDepartment of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA.
Marilyn ChwaDepartment of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA.
Maria Cristina KenneyDepartment of Pathology and Laboratory Medicine, University of California Irvine, Irvine, CA.

Funding

Protective Effects of Humanin on AMD MitochondriaR01EY027363 · NEI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KENNEY, MARIA C · 2019 to 2021
$1.2M
NEI NIH HHS R01 EY027363
6 · The paper itself

Abstract

Purpose: Dry age-related macular degeneration (DAMD) is the leading cause of vision loss in developed countries, yet there are no FDA-approved treatments currently available. Mitochondria play a significant role in the pathology of DAMD; the retinal pigment epithelium cells of patients with DAMD exhibit mitochondrial dysfunction, elevated levels of mitochondrial DNA lesions, and increased mitochondrial reactive oxygen species. Investigations into the mitochondrial contributions to DAMD are complex as human tissue is challenging to acquire, and animal models do not fully recapitulate disease phenotypes. Cytoplasmic hybrid (cybrid) cells, formed by depleting the mitochondria of an immortalized cell line and fusing with patient platelets, are a possible model for mitochondrial studies on DAMD. This study evaluates if cybrid models of DAMD recapitulate the mitochondrial hallmarks of the disease, including mitochondrial dysfunction, decreased mitochondrial protein levels, lipid accumulation, and mitochondrial DNA lesions. Methods: The mitochondrial functions of five healthy and five DAMD cybrid cell lines were compared based on mitochondrial oxygen consumption rates, membrane potential, and protein expression. Secondary factors of mitochondrial dysfunction, including lipid accumulation and mitochondrial DNA stress response, were also examined. Results: Compared to healthy control cybrid lines, we found no alterations in bioenergetics, protein levels, and lipid accumulation in DAMD cybrid lines. Mitochondrial DNA stress responses were aberrant in DAMD cybrids compared to healthy controls, suggesting some conserved mitochondrial dysfunction. Conclusions: Taken together, this study suggests that these DAMD cybrids do not fully recapitulate DAMD mitochondrial pathology, though this is limited to the study population of males with the H mtDNA haplogroup. However, there may be a niche for cybrid cell lines in investigating mitochondrial DNA phenotypes in patients with DAMD. This is likely because DAMD is a multifactorial disease, dependent upon an individual's genetics and the retinal microenvironment.

Indexed as

Geographic AtrophyHybrid CellsMacular DegenerationMitochondriaBlood PlateletsCell LineDNA, MitochondrialHumansMembrane Potential, MitochondrialMitochondrial ProteinsOxygen ConsumptionPhenotypeReactive Oxygen SpeciesRetinal Pigment EpitheliumDNA, MitochondrialMitochondrial ProteinsReactive Oxygen Species

Identifiers

PMID42774060
PMCPMC13585426

What Socratic holds

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Registered trials

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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 Socratic graph.