Evidence map›Paper›PMID 39920300›Full record

ArticleScientific reports2025

Ankrd1 as a potential biomarker for the transition from acute kidney injury to chronic kidney disease.

Hailin Li, Lemei Hu, Changqing Zheng, Ying Kong, Ming Liang, Quhuan Li

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

6 authors.

Hailin Li *School of Biology and Biological Engineering, South China University of Technology, Guangzhou, 510006, Guangdong, China.
Lemei Hu *Department of Nephrology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, People's Republic of China.
Changqing Zheng *School of Biology and Biological Engineering, South China University of Technology, Guangzhou, 510006, Guangdong, China.
Ying KongSchool of Biology and Biological Engineering, South China University of Technology, Guangzhou, 510006, Guangdong, China.
Ming LiangSchool of Medicine, South China University of Technology, Guangzhou, People's Republic of China. eyliangming@scut.edu.cn.
Quhuan LiSchool of Biology and Biological Engineering, South China University of Technology, Guangzhou, 510006, Guangdong, China. liqh@scut.edu.cn.

Funding

National Natural Science Foundation of China 31870928National Natural Science Foundation of China 82170761Natural Science Foundation of Guangdong Province 2021A1515010040
6 · The paper itself

Abstract

Ischemia-reperfusion injury (IRI) is one of the leading causes of acute kidney injury (AKI), predisposing patients to chronic kidney disease (CKD) due to maladaptive renal repair. Nevertheless, the molecular mechanisms and biomarkers that cause maladaptive repair remain unclear. In this study, we used single-nucleus RNA sequencing data from GEO database (GSE139107) to identify molecular markers during the transition from AKI to CKD caused by IRI. Analysis of intercellular crosstalk, trajectory and machine learning algorithms revealed hub cell clusters and genes. Proximal tubule (PT) cells, especially a new cluster (New PT2), significantly interacted with fibroblasts during the transition. The expression levels of hub genes were validated using the bulk RNA-seq data (GSE98622) and further confirmed through RT-qPCR and immunohistochemical analysis in ischemia-reperfusion injury (uIRI) mice. Ankrd1, a hub gene in New PT2, showed sustained upregulation in the proximal tubule in AKI. Compared to the sham-operated group, the expression of Ankrd1 in mice increased at 0.5 days post-reperfusion, peaked at day 1, and remained significantly elevated up to 60 days. This study indicated that the upregulation of Ankrd1 was positively associated with the progression from AKI to CKD and may potentially serve as a valuable biomarker for this transitional process.

Indexed as

Acute Kidney InjuryMuscle ProteinsNuclear ProteinsRenal Insufficiency, ChronicRepressor ProteinsAnimalsBiomarkersDisease Models, AnimalDisease ProgressionHumansKidney Tubules, ProximalMaleMiceMice, Inbred C57BLReperfusion InjuryBiomarkersMuscle ProteinsNuclear ProteinsRepressor ProteinsAcute kidney injuryAnkrd1Chronic kidney diseaseIschemia-reperfusion injuryMaladaptive repair

Identifiers

PMID39920300
PMCPMC11806044

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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.