Evidence map›Paper›PMID 42721961›Full record

ArticleStem cell reports2026

Chemical induction and reversal of photoreceptor dystrophy in retinal organoids.

Allyssa Bradley, Hyejung Min, Soyoung Park, William Temme, Soyeon Park, Ahmad Al-Moujahed, Eun-Jin Lee, Jonathan H Lin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

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

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

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.

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

8 authors.

Allyssa BradleyDepartment of Pathology, School of Medicine, Stanford University, Palo Alto, CA, USA; Department of Ophthalmology, School of Medicine, Stanford University, Palo Alto, CA, USA; VA Palo Alto Health Care System, Department of Veterans Affairs, Veterans Health Administration, Palo Alto, CA, USA.
Hyejung MinDepartment of Pathology, School of Medicine, Stanford University, Palo Alto, CA, USA; Department of Ophthalmology, School of Medicine, Stanford University, Palo Alto, CA, USA; VA Palo Alto Health Care System, Department of Veterans Affairs, Veterans Health Administration, Palo Alto, CA, USA.
Soyoung ParkDepartment of Pathology, School of Medicine, Stanford University, Palo Alto, CA, USA; Department of Ophthalmology, School of Medicine, Stanford University, Palo Alto, CA, USA; VA Palo Alto Health Care System, Department of Veterans Affairs, Veterans Health Administration, Palo Alto, CA, USA.
William TemmeDepartment of Pathology, School of Medicine, Stanford University, Palo Alto, CA, USA; Department of Ophthalmology, School of Medicine, Stanford University, Palo Alto, CA, USA; VA Palo Alto Health Care System, Department of Veterans Affairs, Veterans Health Administration, Palo Alto, CA, USA.
Soyeon ParkDepartment of Pathology, School of Medicine, Stanford University, Palo Alto, CA, USA; Department of Ophthalmology, School of Medicine, Stanford University, Palo Alto, CA, USA.
Ahmad Al-MoujahedDepartment of Ophthalmology, School of Medicine, Stanford University, Palo Alto, CA, USA.
Eun-Jin LeeDepartment of Pathology, School of Medicine, Stanford University, Palo Alto, CA, USA; Department of Ophthalmology, School of Medicine, Stanford University, Palo Alto, CA, USA; VA Palo Alto Health Care System, Department of Veterans Affairs, Veterans Health Administration, Palo Alto, CA, USA.
Jonathan H LinDepartment of Pathology, School of Medicine, Stanford University, Palo Alto, CA, USA; Department of Ophthalmology, School of Medicine, Stanford University, Palo Alto, CA, USA; VA Palo Alto Health Care System, Department of Veterans Affairs, Veterans Health Administration, Palo Alto, CA, USA. Electronic address: jonathan.h.lin@stanford.edu.

Funding

Stanford Vision Research CoreP30EY026877 · NEI · STANFORD UNIVERSITY · PI Jeffrey L Goldberg · 2017 to 2026
$8.0M
Protein Homeostasis and Proteotoxicity MechanismsR01NS088485 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LIN, JONATHAN · 2015 to 2024
$3.0M
NEI NIH HHS P30 EY026877NINDS NIH HHS R01 NS088485RRD VA I01 RX002340
6 · The paper itself

Abstract

Activating transcription factor 6 (ATF6) controls a signal transduction pathway of the unfolded protein response (UPR). Loss-of-function ATF6 mutations cause inherited photoreceptor diseases. Ceapin-A7 is a non-toxic, cell-permeable small molecule that selectively inhibits ATF6. We investigated how ATF6 inhibition impacts photoreceptors by treating wild-type human retinal organoids with Ceapin-A7 and evaluating the effects via single-nucleus RNA sequencing (snRNA-seq) and microscopy after 2 months. Ceapin-A7 administration effectively suppressed ATF6-dependent and UPR-related gene expression and led to fewer rod and cone inner/outer segments, malformed/stunted cone segments, and Müller gliosis, while no photoreceptor cell death was observed. When Ceapin-A7 was removed from retinal organoid media after extended exposure, photoreceptor segment quantity increased, indicating that photoreceptors were able to restore segments. These findings demonstrate that ATF6 is selectively required for photoreceptor inner/outer segment integrity. Furthermore, chemically restoring ATF6 activity promotes photoreceptor segment growth, identifying ATF6/UPR signaling as an attractive pathway to treat photoreceptor diseases.

Indexed as

OrganoidsRetinaActivating Transcription Factor 6HumansSignal TransductionUnfolded Protein ResponseActivating Transcription Factor 6ATF6 protein, humanactivating transcription factor 6ATF6Ceapin-A7photoreceptorretinaretinal organoidunfolded protein responseUPR

Identifiers

PMID42721961
PMCPMC13681322

What OpenQuestion holds

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Read underepoch 390

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 OpenQuestion graph.