Evidence mapPaperPMID 41563806Full record

ArticleJournal of the American Society of Nephrology : JASN2026

Phosphofurin Acidic Cluster Sorting Protein 2 Alleviates Kidney Fibrosis by Inhibiting Tubular Epithelial Cell G2/M Arrest through Cyclin-Dependent Kinase-Like 1.

Chenrui Li, Yan Liu, Hao Zhao, Yiyun Xi, Chongbin Liu, Shilu Luo, Na Jiang, Ming Yang, Yachun Han, Wei Chen and 2 more

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 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. 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

12 authors.

Chenrui LiDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Hunan Key Laboratory of Kidney Disease and Blood Purification, Changsha, Hunan, China.
Yan LiuDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Hunan Key Laboratory of Kidney Disease and Blood Purification, Changsha, Hunan, China.
Hao ZhaoDepartment of Radiation Oncology, Chongqing University Cancer Hospital, Chongqing, China.
Yiyun XiDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Hunan Key Laboratory of Kidney Disease and Blood Purification, Changsha, Hunan, China.
Chongbin LiuDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Hunan Key Laboratory of Kidney Disease and Blood Purification, Changsha, Hunan, China.ORCID 0009-0000-5451-0338
Shilu LuoDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Hunan Key Laboratory of Kidney Disease and Blood Purification, Changsha, Hunan, China.
Na JiangDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Hunan Key Laboratory of Kidney Disease and Blood Purification, Changsha, Hunan, China.
Ming YangDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Hunan Key Laboratory of Kidney Disease and Blood Purification, Changsha, Hunan, China.ORCID 0000-0003-1698-0616
Yachun HanDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Hunan Key Laboratory of Kidney Disease and Blood Purification, Changsha, Hunan, China.
Wei ChenDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Hunan Key Laboratory of Kidney Disease and Blood Purification, Changsha, Hunan, China.
Li LiDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Hunan Key Laboratory of Kidney Disease and Blood Purification, Changsha, Hunan, China.
Lin SunDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Hunan Key Laboratory of Kidney Disease and Blood Purification, Changsha, Hunan, China.ORCID 0000-0002-4544-0822

Funding

National Natural Science Foundation of China 81730018National Natural Science Foundation of China 82300828National Natural Science Foundation of China 82370730National Natural Science Foundation of China 82400805
6 · The paper itself

Abstract

key pointsPhosphofurin acidic cluster sorting protein 2 (PACS-2) expression was lower in fibrotic kidney tubule, and proximal tubule-specific deficiency accelerated the progression of CKD. PACS-2 deficiency exacerbated G2/M cell cycle arrest in proximal tubular cells to promote kidney fibrosis. PACS-2 interacted with cyclin-dependent kinase-like 1 and modulated its kinase activity, thereby regulating cell cycle progression.

backgroundKidney fibrosis is the final common pathway of CKD. Proximal tubular epithelial cells (PTECs) arrested in G2/M phase of the cell cycle play a pivotal role in kidney fibrosis. Phosphofurin acidic cluster sorting protein 2 (PACS-2) is a multifunctional protein involved in various cellular activities including cell cycle regulation, yet its role in kidney fibrosis remains unclear.

methodsPTEC-specific Pacs-2 knockout mice were generated by using LoxP-Cre recombination system and subjected to unilateral ureteral obstruction (UUO) and aristolochic acid to induce kidney fibrosis. Cultured human and mouse tubular epithelial cells were treated with TGF- β 1 to analyze the underlying cellular mechanisms. Coimmunoprecipitation coupled with mass spectrometry, molecular cloning, and genetic manipulation were used to investigate PACS-2 interactions and specific binding domains.

resultsPACS-2 expression was significantly lower in the cortex of fibrotic kidney from UUO mouse. PACS-2 deficiency in PTECs exacerbated G2/M cell cycle arrest and kidney fibrosis in murine UUO and aristolochic acid nephropathy models, two independent models for CKD. In vitro , overexpression of PACS-2 alleviated TGF- β 1-induced fibrogenic responses in PTECs through inhibiting cell cycle arrest at G2/M phase. By coimmunoprecipitation coupled with mass spectrometry, we identified cyclin-dependent kinase-like 1 (CDKL1) as the key molecule linking PACS-2 to cell cycle progression in PTECs. Knockdown of CDKL1 partially reversed the antifibrotic effects of PACS-2 by promoting G2/M cell cycle arrest in TGF- β 1-stimulated HK-2 cells. Mechanistically, we demonstrated that PACS-2 interacted with kinase domain of CDKL1 and modulated its kinase activity, thereby regulating cell cycle, rather than affecting its subcellular translocation or protein expression.

conclusionsOur study demonstrates that renal tubular PACS-2 alleviated G2/M cell cycle arrest and kidney fibrosis by interacting with CDKL1 and modulating its kinase activity.

Indexed as

Epithelial CellsG2 Phase Cell Cycle CheckpointsKidneyKidney Tubules, ProximalAnimalsCells, CulturedFibrosisHumansKidney TubulesMaleMiceMice, KnockoutCKDkinaserenal fibrosisrenal tubular epithelial cells

Identifiers

PMID41563806
PMCPMC13143453

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.