Evidence map›Paper›PMID 42365006›Full record

ArticleNature communications2026

NAD+ modulates mitochondrial vulnerability in MERTK-associated models of retinitis pigmentosa.

Lujia Feng, Yuwen Wen, Ting Zhang, Xiaohua Zhuo, Yantao Wei, Lixian Liu, Zhaohao Huang, Guoming Zhang, Lu Chen, Yong Du and 15 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 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

25 authors.

Lujia Feng *Shenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China.
Yuwen Wen *State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China.
Ting Zhang *State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China.
Xiaohua ZhuoShenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China.
Yantao WeiState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China.
Lixian LiuShenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China.
Zhaohao HuangState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China.
Guoming ZhangShenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China.
Lu ChenShenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China.
Yong DuShenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China.
Dong FangShenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China.
Wangting LiShenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China.
Linbin ZhouState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China.
Ling ZhaoState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China.
Yingting ZhuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China.
Jia LiangShenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China.
Zhiquan LiState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China.
Xiaojing SongState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China.
Caibin DengState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China.
Xingxing MaoShenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China.
Xiaofeng HouShenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China.
Wenru SuDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. suwenru@sjtu.edu.cn.
Wei ChiShenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China. chiwei@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-7424-3879
Yehong ZhuoState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China. zhuoyh@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0003-3247-7199
Shaochong ZhangShenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, China. zhangshaochong@gzzoc.com.ORCID http://orcid.org/0000-0002-2212-7139

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinitis pigmentosa (RP) is the most common inherited retinal degenerative disease leading to blindness. RP is characterized by progressive loss of photoreceptors and retinal pigment epithelium (RPE), leading to retinal degeneration. The mechanisms that initiate RP and drive retinal vulnerability are poorly understood, and new strategies for preventing and treating RP are urgently needed. Although mitochondrial dysfunction initiates many neurodegenerative diseases, the contribution of mitochondrial dysfunction to RP is unclear. Single-cell RNA sequencing, transmission electron microscopy, and enzyme-linked immunosorbent assays revealed that photoreceptor and RPE cells have abnormal mitochondria in rats with RP. Nicotinamide adenine dinucleotide (NAD+) metabolism decreased in rats with RP, increasing the vulnerability to disease-related insults. Similar experimental results were observed in a Mer tyrosine kinase receptor (MERTK)-associated RP primary human RPE cell model. Electroretinography, immunofluorescence, and fundus photography revealed that oral administration of the NAD+ precursor nicotinamide mononucleotide (NMN) protected rats with RP from retinal degeneration. Single-cell RNA sequencing, siRNA targeting, and Adeno-associated virus applications demonstrated that NMN elicits therapeutic effects via the glyceraldehyde-phosphate dehydrogenase-mitochondria pathway. These results indicate that mitochondrial abnormalities may be drivers of RP, and NMN elicits therapeutic effects on RP.

Indexed as

c-Mer Tyrosine KinaseMitochondriaNADRetinitis PigmentosaAnimalsDisease Models, AnimalElectroretinographyHumansMaleRatsRats, Sprague-DawleyRetinal Pigment Epitheliumc-Mer Tyrosine KinaseNAD

Identifiers

PMID42365006
PMCPMC13454435

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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.