Evidence map›Paper›PMID 39725005›Full record

ArticleJournal of advanced research2025

Loss of glomerular aldolase B in diabetic nephropathy promotes renal fibrosis via activating Akt/GSK/β-catenin axis.

Minghui Liu, Wenwen Yang, Shuang Qu, Tingting Zhao, Song Jiang, Suming Peng, Mingchao Zhang, Ji Xuan, Zhihong Liu, Ke Zen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2025. 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. 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

10 authors.

Minghui LiuSchool of Pharmaceutical Science, Nanjing Tech University, 30 South Puzhu Road, Nanjing, Jiangsu 211816, China; State Key Laboratory of Pharmaceutical Biotechnology, Department of Gastroenterology, Drum Tower Hospital, Nanjing University, School of Life Sciences, Nanjing, Jiangsu 210093, China.
Wenwen YangState Key Laboratory of Pharmaceutical Biotechnology, Department of Gastroenterology, Drum Tower Hospital, Nanjing University, School of Life Sciences, Nanjing, Jiangsu 210093, China.
Shuang QuGeriatric Hospital of Nanjing Medical University, Nanjing, Jiangsu 210024, China.
Tingting ZhaoNational Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu 210002, China.
Song JiangNational Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu 210002, China.
Suming PengSchool of Life Science and Technology, Chinese Pharmaceutical University, Nanjing, Jiangsu 211198, China.
Mingchao ZhangNational Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu 210002, China.
Ji XuanDepartment of Gastroenterology, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, Jiangsu 210002, China. Electronic address: helio0009@126.com.
Zhihong LiuNational Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu 210002, China. Electronic address: liuzhihong@nju.edu.cn.
Ke ZenState Key Laboratory of Pharmaceutical Biotechnology, Department of Gastroenterology, Drum Tower Hospital, Nanjing University, School of Life Sciences, Nanjing, Jiangsu 210093, China. Electronic address: kzen@nju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveDiabetic nephropathy (DN), characterized by a complex and multifaceted pathogenesis, stands as the foremost catalyst behind end-stage renal disease (ESRD). This study aims to analyze the level and non-metabolic role of glomerular aldolase B (ALDOB) in DN progression.

methodsGlomerular proteomics and transcriptome are analyzed from 50 DN patients and 25 controls, respectively. Human kidney biopsy, cultured podocytes and mouse models are employed to study ALDOB levels and function.

resultsALDOB is strongly downregulated in DN-affected glomeruli, as well as in human and murine podocytes exposed to inflammatory cytokines. ALDOB reduction increases podocyte injury, while adenovirus-mediated ALDOB overexpression leads to substantial alleviation of renal injuries in a diabetic mouse model. Mechanistically, ALDOB reduction triggers the Akt/GSK/β-catenin signaling cascade within podocytes.

conclusionOur findings reveal a novel non-metabolic role of glomerular ALDOB in protecting against podocyte injury and renal fibrosis.

Indexed as

beta CateninDiabetic NephropathiesFructose-Bisphosphate AldolaseKidney GlomerulusProto-Oncogene Proteins c-aktAnimalsDisease Models, AnimalFemaleFibrosisHumansMaleMiceMiddle AgedPodocytesSignal Transductionbeta CateninFructose-Bisphosphate AldolaseProto-Oncogene Proteins c-aktAkt/GSK/β-catenin axisALDOBDiabetic nephropathyGlomerulusRenal fibrosis

Identifiers

PMID39725005
PMCPMC12793748

What OpenQuestion holds

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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 OpenQuestion graph.