Evidence map›Paper›PMID 39083268›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Forkhead Box Protein K1 Promotes Chronic Kidney Disease by Driving Glycolysis in Tubular Epithelial Cells.

Lu Zhang, Maoqing Tian, Meng Zhang, Chen Li, Xiaofei Wang, Yuyu Long, Yujuan Wang, Jijia Hu, Cheng Chen, Xinghua Chen and 5 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Article
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  5. Article
  6. Review
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  9. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Autophagy · 2026
    Article
  16. Article
  17. Article
  18. Review
  19. Tubular ACSM3 deficiency impairs medium-chain fatty acid metabolism and aggravates kidney fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. 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

15 authors.

Lu ZhangDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Maoqing TianDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Meng ZhangDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Chen LiDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Xiaofei WangDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Yuyu LongDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Yujuan WangDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Jijia HuDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Cheng ChenDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Xinghua ChenDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Wei LiangDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Guohua DingDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Hua GanDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Lunzhi LiuHubei Provincial Clinical Medical Research Center for Nephropathy, Minda Hospital of Hubei Minzu University, Enshi, Hubei, 445000, China.
Huiming WangDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.ORCID 0000-0002-1706-2342

Funding

China Social Welfare Foundation SLB-6-20210323-99Department of Science and Technology, Hubei Provincial People's Government 2019ACA137National Natural Science Foundation of China 81800614National Natural Science Foundation of China 82270711National Natural Science Foundation of China 82370682
6 · The paper itself

Abstract

Renal tubular epithelial cells (TECs) undergo an energy-related metabolic shift from fatty acid oxidation to glycolysis during chronic kidney disease (CKD) progression. However, the mechanisms underlying this burst of glycolysis remain unclear. Herein, a new critical glycolysis regulator, the transcription factor forkhead box protein K1 (FOXK1) that is expressed in TECs during renal fibrosis and exhibits fibrogenic and metabolism-rewiring capacities is reported. Genetic modification of the Foxk1 locus in TECs alters glycolytic metabolism and fibrotic lesions. A surge in the expression of a set of glycolysis-related genes following FOXK1 protein activation contributes to the energy-related metabolic shift. Nuclear-translocated FOXK1 forms condensate through liquid-liquid phase separation (LLPS) to drive the transcription of target genes. Core intrinsically disordered regions within FOXK1 protein are mapped and validated. A therapeutic strategy is explored by targeting the Foxk1 locus in a murine model of CKD by the renal subcapsular injection of a recombinant adeno-associated virus 9 vector encoding Foxk1-short hairpin RNA. In summary, the mechanism of a FOXK1-mediated glycolytic burst in TECs, which involves the LLPS to enhance FOXK1 transcriptional activity is elucidated.

Indexed as

Disease Models, AnimalEpithelial CellsForkhead Transcription FactorsGlycolysisRenal Insufficiency, ChronicAnimalsHumansKidney TubulesMiceMice, Inbred C57BLForkhead Transcription FactorsFoxk1 protein, mousechronic kidney diseaseFOXK1glycolysisphase separationtranscriptional regulation

Identifiers

PMID39083268
PMCPMC11423168

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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.