Evidence map›Paper›PMID 39602004›Full record

ArticleInternational urology and nephrology2025

Sulforaphane alleviates renal fibrosis through dual regulation on mTOR-mediated autophagy pathway.

Di Zhang, Han Zhang, Shiqi Lv, Cheng Zhu, Shaomin Gong, Xixi Yu, Yulin Wang, Xinhui Huang, ShuangXin Yuan, Xiaoqiang Ding and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in International urology and nephrology, 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

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. Article
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

11 authors.

Di Zhang *Department of Nephrology, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Shanghai, 200032, China.
Han Zhang *Department of Nephrology, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Shanghai, 200032, China.
Shiqi LvDepartment of Nephrology, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Shanghai, 200032, China.
Cheng ZhuDepartment of Nephrology, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Shanghai, 200032, China.
Shaomin GongDepartment of Nephrology, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Shanghai, 200032, China.
Xixi YuDepartment of Nephrology, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Shanghai, 200032, China.
Yulin WangDepartment of Nephrology, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Shanghai, 200032, China.
Xinhui HuangDepartment of Nephrology, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Shanghai, 200032, China.
ShuangXin YuanDepartment of Nephrology, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Shanghai, 200032, China.
Xiaoqiang DingDepartment of Nephrology, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Shanghai, 200032, China. ding.xiaoqiang@zs-hospital.sh.cn.
Xiaoyan ZhangDepartment of Nephrology, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Shanghai, 200032, China. zhang.xiaoyan@zs-hospital.sh.cn.

Funding

National Natural Science Foundation of China 82170752
6 · The paper itself

Abstract

Renal fibrosis is a common pathological process of progressive chronic kidney disease (CKD). However, effective therapy is constrained currently. Autophagy is an important mechanism in kidney injury and repairment but its exact role in renal fibrosis was discrepant according to previous studies. Sulforaphane (SFN), a natural plant compound, has been explored as a promising nutritional therapy for a variety of diseases. But the salutary effect and underlying mechanism of SFN on CKD have not been fully elucidated. In this study, we investigated the effect of SFN on renal fibrosis in unilateral ureteral obstruction (UUO) mice. Then we examined the regulatory effect of SFN on autophagy-related proteins in renal fibroblasts and renal tubular epithelial cells. Our results showed that sulforaphane could significantly alleviate renal fibrosis in UUO mice. In vitro, the expression levels of autophagy-related protein showed that SFN could upregulate the autophagy activity of renal interstitial fibroblasts and downregulate the autophagy activity of renal tubular epithelial cells. Furthermore, we found that phosphorylated mTOR protein levels was reduced in renal fibroblasts and increased in renal tubular epithelial cells after SFN treatment. Our results strongly suggested that SFN could alleviate renal fibrosis through dual regulation of mTOR-mediated autophagy pathway. This finding may provide a new perspective on the renal salutary effect of SFN and provide a preclinical rationale for exploring the therapeutic potential of SFN to slow down renal fibrosis.

Indexed as

AutophagyIsothiocyanatesKidneyTOR Serine-Threonine KinasesAnimalsDisease Models, AnimalFibroblastsFibrosisMaleMiceMice, Inbred C57BLSignal TransductionSulfoxidesUreteral ObstructionIsothiocyanatesmTOR protein, mousesulforaphaneSulfoxidesTOR Serine-Threonine KinasesAutophagymTORRenal fibrosisSulforaphane

Identifiers

PMID39602004

What OpenQuestion holds

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Registered trials

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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.