Evidence map›Paper›PMID 41719329›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2026

DAPL1 restrains RPE PANoptosis in experimental AMD by inhibiting GRP75-mediated mitochondria-associated endoplasmic reticulum membranes.

Yan Li, Meiyu Jing, Wanxiao Wang, Wanzhen Lin, Yingxin Zhang, Tianyin Nie, Pingping Liu, Wan-Ni Lu, Yu Chen, J Fielding Hejtmancik and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

13 authors.

Yan LiLaboratory of Developmental Cell Biology and Disease, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Meiyu JingLaboratory of Developmental Cell Biology and Disease, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Wanxiao WangLaboratory of Developmental Cell Biology and Disease, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Wanzhen LinLaboratory of Developmental Cell Biology and Disease, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.ORCID 0009-0002-5454-1171
Yingxin ZhangLaboratory of Developmental Cell Biology and Disease, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Tianyin NieLaboratory of Developmental Cell Biology and Disease, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Pingping LiuLaboratory of Developmental Cell Biology and Disease, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Wan-Ni LuLaboratory of Developmental Cell Biology and Disease, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Yu ChenLaboratory of Developmental Cell Biology and Disease, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
J Fielding HejtmancikOphthalmic Molecular Genetics Section, Ophthalmic Genetics and Visual Function Branch, National Eye Institute, NIH, Bethesda, MD 20892.ORCID 0009-0009-9144-7951
Qinxiang ZhengNational Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Ling HouLaboratory of Developmental Cell Biology and Disease, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.ORCID 0000-0003-0705-8099
Xiaoyin MaLaboratory of Developmental Cell Biology and Disease, State Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.ORCID 0000-0002-3564-1647

Funding

MOST | National Key Research and Development Program of China (NKPs) 2023YFC2506100MOST | National Natural Science Foundation of China (NSFC) 82171065MOST | National Natural Science Foundation of China (NSFC) 82371081MOST | National Natural Science Foundation of China (NSFC) 82571231
6 · The paper itself

Abstract

Retinal pigment epithelium (RPE) cell damage is a critical factor of age-related macular degeneration (AMD), the leading cause of blindness among the aged population. This study focuses on the AMD susceptible gene, Death associated protein like 1 (DAPL1), and provides insights with significant therapeutic implications. DAPL1-deficient mice exhibit dry AMD-like pathological features, a phenomenon whose mechanisms have remained largely unknown. Here, we reveal that DAPL1 deficiency promotes the formation of mitochondria-associated endoplasmic reticulum membranes (MAMs) to cause mitochondrial Ca

Indexed as

Apoptosis Regulatory ProteinsEndoplasmic ReticulumHSP70 Heat-Shock ProteinsMacular DegenerationMembrane ProteinsRetinal Pigment EpitheliumAnimalsApoptosisCalciumDisease Models, AnimalHumansMiceMice, KnockoutMitochondriaMitochondria Associated MembranesApoptosis Regulatory ProteinsCalciumglucose-regulated proteinsHSP70 Heat-Shock ProteinsMembrane ProteinsAMDGRP75mitochondria-associated ER membranePANoptosisRPE

Identifiers

PMID41719329
PMCPMC12933084

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.