Evidence map›Paper›PMID 42567988›Full record

ArticleNature cell biology2026

The mitochondria enzyme OGDH defends against disulfidptosis by licensing METTL3-regulated NRF2 translation.

Xiao-Yan Chen, Ke-Jun Xu, Jia-Xin Zhou, Liu-Zheng Wu, De-Yi Feng, Yun-Feng Guan, Heng-Hui Li, Guang-Xi Yang, Yu Qian, Meng-Hao Mi and 5 more

Abstract read
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Article in Nature cell biology, 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

15 authors.

Xiao-Yan Chen *State Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.
Ke-Jun Xu *State Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.
Jia-Xin Zhou *State Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.
Liu-Zheng Wu *State Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.
De-Yi FengState Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.ORCID http://orcid.org/0000-0003-1837-1320
Yun-Feng GuanState Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.
Heng-Hui LiState Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.
Guang-Xi YangState Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.
Yu QianState Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.
Meng-Hao MiState Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.
Sheng-Fu WuState Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.
Zhi-Yuan ZhangState Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.
Qi-Tao ChenState Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.ORCID http://orcid.org/0009-0001-8118-4520
Bo ZhouState Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China.
Hang-Zi ChenState Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Xiamen University, Xiamen, China. chenhz@xmu.edu.cn.ORCID http://orcid.org/0000-0002-4827-2182

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32170777National Natural Science Foundation of China (National Science Foundation of China) U23A20450
6 · The paper itself

Abstract

Disulfidptosis is a form of regulated cell death triggered by disulfide stress resulting from glucose starvation. The capacity to evade disulfidptosis is crucial for tumour cells to withstand glucose-limited environments. Here we demonstrate that OGDH, a rate-limiting enzyme in citric acid cycle, is critical for conferring resistance to disulfidptosis. High expression of HSPA9 in melanoma protects OGDH from glucose deprivation-induced oxidative inactivation, thereby ensuring OGDH-generated succinyl-CoA for METTL3 succinylation. Succinylated METTL3 recognizes m

Indexed as

DisulfidptosisMelanomaMethyltransferasesMitochondriaNF-E2-Related Factor 2Protein BiosynthesisAnimalsCell Line, TumorGlucoseHSP70 Heat-Shock ProteinsHumansMiceRNA MethylationSignal TransductionThioredoxin Reductase 1GlucoseHSP70 Heat-Shock ProteinsMethyltransferasesNFE2L2 protein, humanNfe2l2 protein, mouseNF-E2-Related Factor 2Thioredoxin Reductase 1TXNRD1 protein, human

Identifiers

What Socratic holds

Textmetadata
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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 Socratic graph.