NRF2 Deficiency Disrupts Mitochondrial Homeostasis via NDUFS7 in Trabecular Meshwork.

Xuejing Yan, Shen Wu, Xiaowei Fan, Qian Li, Yufei Teng, Ningli Wang, Jingxue Zhang

Abstract read

In one paragraph

Article in Research (Washington, D.C.), 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

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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

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Xuejing YanBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Intelligent Diagnosis Technology and Equipment for Optic Nerve-Related Eye Diseases, Capital Medical University, Beijing 100730, China.ORCID https://orcid.org/0000-0002-1500-9193

Shen WuBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Intelligent Diagnosis Technology and Equipment for Optic Nerve-Related Eye Diseases, Capital Medical University, Beijing 100730, China.

Xiaowei FanBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Intelligent Diagnosis Technology and Equipment for Optic Nerve-Related Eye Diseases, Capital Medical University, Beijing 100730, China.

Qian LiBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Intelligent Diagnosis Technology and Equipment for Optic Nerve-Related Eye Diseases, Capital Medical University, Beijing 100730, China.

Yufei TengBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Intelligent Diagnosis Technology and Equipment for Optic Nerve-Related Eye Diseases, Capital Medical University, Beijing 100730, China.

Ningli WangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Intelligent Diagnosis Technology and Equipment for Optic Nerve-Related Eye Diseases, Capital Medical University, Beijing 100730, China.

Jingxue ZhangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Intelligent Diagnosis Technology and Equipment for Optic Nerve-Related Eye Diseases, Capital Medical University, Beijing 100730, China.ORCID https://orcid.org/0000-0002-9512-9602

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The trabecular meshwork (TM) plays a pivotal role in maintaining intraocular pressure (IOP) by regulating aqueous humor outflow. Nuclear factor erythroid 2-related factor 2 (NRF2) was identified as a key transcriptional controller of TM redox balance and mitochondrial function. Transcriptomic profiling of tert-butyl hydroperoxide (tBHP)-induced oxidative injury revealed NRF2 pathway involvement in TM cellular defense. NRF2 knockout (KO) mice exhibited impaired aqueous humor dynamics, elevated IOP, and TM oxidative damage. In vitro, NRF2 knockdown aggravated oxidative stress and mitochondrial dysfunction, whereas NRF2 overexpression mitigated tBHP-induced cytotoxicity. The results of the gene set enrichment analysis (GSEA) indicated enrichment of oxidative phosphorylation pathway in NRF2-deficient cells. Chromatin immunoprecipitation sequencing (ChIP-seq) confirmed NDUFS7 as a direct NRF2 target essential for mitochondrial complex I integrity. Restoration of NDUFS7 expression in NRF2-deficient TM cells or KO mice rescued mitochondrial impairment. Collectively, these findings establish the NRF2/NDUFS7 axis as a central defense mechanism protecting TM from oxidative injury and suggest potential therapeutic strategies for glaucoma-associated ocular hypertension.

Identifiers

PMID41869290

DOI10.34133/research.1203

PMCPMC13003157

What Socratic holds

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LicenceCC BY

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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.