Evidence map›Paper›PMID 41334440›Full record

ArticleFrontiers in endocrinology2025

PSCP, a novel reactive sulfur donor, activates Keap1-Nrf2 signaling and attenuates mitochondrial dysfunction in diabetic retinopathy.

Kexin Li, Ruiying Ji, Youbang Chen, Yiwen Wang, Yiyan Guo, Xiang Li, Hui Zhang, Liang Guo, Chun-Tao Yang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in endocrinology, 2025. 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

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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

9 authors.

Kexin Li *Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Ruiying Ji *Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Youbang Chen *Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Yiwen WangGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Yiyan GuoGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Xiang LiGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Hui ZhangGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Liang GuoSchool of Exercise and Health and Collaborative Innovation Center for Sports and Public Health, Shanghai University of Sport, Shanghai, China.
Chun-Tao YangGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Diabetic retinopathy (DR) is a leading cause of vision loss in diabetes, yet its underlying molecular drivers remain poorly defined. This study aimed to identify diabetic stress-responsive targets and explore the therapeutic potential of the reactive sulfur donor PSCP by integrating transcriptomic and functional analyses in diabetic mouse and cell models. Methods: Retinal transcriptomic datasets from type 1 and type 2 diabetic mice (GSE111465 and GSE55389) were analyzed for mitochondrial and antioxidant gene expression. Results: Transcriptomic analysis revealed consistent dysregulation of mitochondrial antioxidant enzymes IDH2 and MGST1 in diabetic retinas. Oxidative and carbonyl stress in ARPE-19 cells led to reactive oxygen species accumulation, loss of mitochondrial membrane potential, and reduced cell viability, accompanied by suppression of IDH2 and MGST1. PSCP treatment induced Keap1 modification and promoted Nrf2 nuclear translocation, restoring the expression of IDH2, MGST1, and mitochondrial dynamics regulators MFN2 and FIS1. PSCP also preserved mitochondrial membrane potential and improved cell survival. This protective effect was abrogated by ML385. Conclusions: Our findings identify IDH2 and MGST1 as stress-responsive mitochondrial targets in DR and demonstrate that PSCP activates the Keap1-Nrf2 pathway to preserve mitochondrial integrity under diabetic stress.

Indexed as

Diabetic RetinopathyKelch-Like ECH-Associated Protein 1MitochondriaNF-E2-Related Factor 2AnimalsDiabetes Mellitus, ExperimentalHumansMaleMiceMice, Inbred C57BLOxidative StressSignal TransductionKeap1 protein, mouseKelch-Like ECH-Associated Protein 1Nfe2l2 protein, mouseNF-E2-Related Factor 2diabetic retinopathyIDH2Keap1-Nrf2 pathwayMGST1mitochondrial dysfunctionreactive sulfur species

Identifiers

PMID41334440
PMCPMC12665532

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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.