Evidence map›Paper›PMID 41474228›Full record

ArticleJournal of cellular and molecular medicine2026

Novel Roles of GDF15 in Alleviating Renal Fibrosis: Promoting Autophagy and Lysosome Biogenesis via Inhibition of the PI3K/Akt/mTOR Pathway.

Youqi Li, Jinge Gu, Danping Tao, Haoyang Wu, Chen Yang, Yongjun Shi, Chengwen Huang, Boxun Luo, Jun Zhang

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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.

Youqi LiDepartment of Nephrology, Huizhou Central People's Hospital, Huizhou, Guangdong, China.ORCID https://orcid.org/0000-0002-5644-372X
Jinge GuDepartment of Nephrology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Danping TaoDepartment of Gerontology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Haoyang WuDepartment of Otolaryngology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Chen YangKey Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Yongjun ShiDepartment of Nephrology, Huizhou Central People's Hospital, Huizhou, Guangdong, China.
Chengwen HuangDepartment of Nephrology, Huizhou Central People's Hospital, Huizhou, Guangdong, China.
Boxun LuoDepartment of Nephrology, Huizhou Central People's Hospital, Huizhou, Guangdong, China.
Jun ZhangDepartment of Nephrology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.

Funding

Medical Scientific Research Foundation of Guangdong Province B2023382Natural Science Foundation of Guangdong Province 2021A1515012175Natural Science Foundation of Guangdong Province 2024A1515010402
6 · The paper itself

Abstract

Tubulointerstitial fibrosis (TIF) significantly contributes to the development of end-stage renal disease (ESRD) in chronic kidney disease (CKD). However, the underlying mechanisms driving its development remain poorly understood, thereby impeding the development of effective prevention and treatment strategies. Although growth differentiation factor 15 (GDF15) has been implicated in kidney diseases, its specific relationship and mechanisms in the context of renal TIF remain unclear. In this study, we investigated the role and mechanisms of GDF15 in TIF using a mouse model of unilateral ureteral obstruction (UUO) and human tubular epithelial cells (HK2) stimulated by transforming growth factor-β1 (TGF-β1). Our findings demonstrated a downregulation of GDF15 expression in TIF. The upregulation of GDF15 mitigates renal TIF and reduces macrophage infiltration, whereas its downregulation exacerbates these conditions. Further analysis revealed that GDF15 promotes autophagy and lysosome biogenesis via the PI3K/Akt/mTOR signalling pathway, conferring a protective effect against TIF. In summary, our study demonstrated a negative correlation between GDF15 expression and renal TIF, highlighting its protective role in TIF. Moreover, GDF15 was found to promote autophagy and resolution of TIF through the PI3K/Akt/mTOR signalling pathway.

Indexed as

AutophagyGrowth Differentiation Factor 15Kidney DiseasesLysosomesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAnimalsCell LineDisease Models, AnimalFibrosisHumansKidneyMaleMiceMice, Inbred C57BLGDF15 protein, humanGdf15 protein, mouseGrowth Differentiation Factor 15Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTransforming Growth Factor beta1autophagyGDF15macrophage infiltrationPI3K/Akt/mTOR pathwaytubulointerstitial fibrosis

Identifiers

PMID41474228
PMCPMC12755054

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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.