Evidence map›Paper›PMID 41696093›Full record

ArticleWorld journal of diabetes2026

Fibroblast growth factor 1 alleviates diabetic nephropathy by reducing renal lipid accumulation in diabetic kidney.

Ying-Jian Li, He-Yu Ge, Gui-Gui Zhang, Hao-Yu Chen, Yu-Jia Xi, Kai Wang, Yin-Li Huang, Chi Zhang, Xia Fan, Xiao-Qing Yan

Abstract read
In one paragraph

Article in World journal of diabetes, 2026. 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. 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

10 authors.

Ying-Jian LiDepartment of Endocrinology, Pingyang Hospital of Wenzhou Medical University, Wenzhou 325499, Zhejiang Province, China.
He-Yu GeSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang Province, China.
Gui-Gui ZhangSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang Province, China.
Hao-Yu ChenSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang Province, China.
Yu-Jia XiSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang Province, China.
Kai WangDepartment of Cardiology, Heart Center, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China.
Yin-Li HuangDepartment of Endocrinology, Pingyang Hospital of Wenzhou Medical University, Wenzhou 325499, Zhejiang Province, China.
Chi ZhangWenzhou Key Laboratory for The Diagnosis and Prevention of Diabetic Complications, The Third Affiliated Hospital of Wenzhou Medical University (Ruian People's Hospital), Wenzhou 325200, Zhejiang Province, China.
Xia FanSchool and Hospital of Stomatology, Wenzhou Medical University, Wenzhou 325027, Zhejiang Province, China.
Xiao-Qing YanDepartment of Endocrinology, Pingyang Hospital of Wenzhou Medical University, Wenzhou 325499, Zhejiang Province, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic nephropathy (DN) is a major complication of diabetes, yet therapeutic strategies that specifically target its pathogenesis are still lacking.

aimTo evaluate the therapeutic potential of fibroblast growth factor 1 (FGF1) in DN and explore its underlying mechanisms.

methodsDN was induced

resultsFGF1 treatment reduced urinary albumin excretion, ameliorated glomerular hypertrophy, attenuated renal fibrosis and inflammation, and diminished lipid accumulation in diabetic kidneys. Analysis of fatty acid metabolism revealed that cluster of differentiation 36, a key regulator of long-chain fatty acids uptake, was upregulated, while carnitine palmitoyl transferase 1A, a rate-limiting enzyme in fatty acid beta-oxidation (FAO), was downregulated in diabetic kidneys and HGPA-treated HK-2 cells. FGF1 treatment normalized the expression of both cluster of differentiation 36 and carnitine palmitoyl transferase 1A and enhanced FAO in HGPA-treated HK-2 cells. Mechanistically, FGF1 restored AMP-activated protein kinase (AMPK) activity and peroxisome proliferator-activated receptor alpha expression, both of which were suppressed in DN and HGPA-treated HK-2 cells. Notably, pharmacological inhibition of AMPK or FAO abolished the protective effect of FGF1.

conclusionFGF1 alleviates DN by inhibiting fatty acid uptake and promoting lipid catabolism

Indexed as

AMP-activated protein kinaseCarnitine palmitoyl transferase 1ADiabetic nephropathyFibroblast growth factor 1Human kidney-2Lipid accumulation

Identifiers

PMID41696093
PMCPMC12897520

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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.