Evidence map›Paper›PMID 32571212›Full record

ArticleBMC molecular and cell biology2020

Klotho is regulated by transcription factor Sp1 in renal tubular epithelial cells.

Yan Li, Yong Liu, Kailong Wang, Yinghui Huang, Wenhao Han, Jiachuan Xiong, Ke Yang, Mingying Liu, Tangli Xiao, Chi Liu and 5 more

Open access · goldAbstract read
In one paragraph

Article in BMC molecular and cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Exogenous Klotho Extends Survival in COVID-19 Model Mice.Pathogens (Basel, Switzerland) · 2023
    Article
  11. Role of Klotho Protein in Neuropsychiatric Disorders: A Narrative Review.Indian journal of clinical biochemistry : IJCB · 2023
    Review
  12. Magnesium in renal fibrosis.International urology and nephrology · 2022
    Review
  13. CCL5 Suppresses Klotho ExpressionFrontiers in physiology · 2022
    Article
  14. 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

15 authors at 1 institution in 1 country.

Yan LiDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Yong LiuDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Kailong WangDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Yinghui HuangDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Wenhao HanDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Jiachuan XiongDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Ke YangDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Mingying LiuDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Tangli XiaoDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Chi LiuDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Ting HeDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Xianjin BiDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Jingbo ZhangDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Bo ZhangDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China.
Jinghong ZhaoDepartment of Nephrology, the key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Kidney Center of PLA, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, People's Republic of China. zhaojh@tmmu.edu.cn.ORCID http://orcid.org/0000-0001-9750-3285
Army Medical University · CN

Funding

Frontier specific projects of Xinqiao Hospital 2018YQYLY004National Key R&D Program of China 2017YFA0106600National Key R&D Program of China 2018YFC1312700Personnal training Program for Clinical Medicine Research of Army Medical University 2018XLC1007the Natural Science Foundation of China 81500544the Natural Science Foundation of China 81500561the Natural Science Foundation of China 81800616the Natural Science Foundation of China 81800621the Natural Science Foundation of China 81873605
6 · The paper itself

Abstract

backgroundKlotho is a multifunctional protein, which exists both in a membrane bound and a soluble form. In renal tubules, Klotho is involved in cell senescence, anti-oxidant response, and renal fibrosis, thus regulation of its expression is critical to understand its roles in renal diseases. Indeed, reduced expression was observed in various renal disease. However, the mechanisms underlying transcriptional regulation of the human klotho gene (KL) largely remain unknown.

resultsHere we demonstrated that the Klotho expression in human renal tubular epithelial cells (RTECs) was enhanced by overexpression of the transcription factor Sp1. On the contrary, Klotho expression was decreased by Sp1 knockdown. Besides, increased expression of Sp1 alleviated TGF-β1-induced fibrosis in HK-2 cells by inducing Klotho expression. Luciferase reporter assays and chromatin immunoprecipitation assays further identified the binding site of Sp1 was located in - 394 to - 289 nt of the KL promoter, which was further confirmed by mutation analysis.

conclusionsThese data demonstrate that KL is a transcriptional target of Sp1 and TGF-β1-induced fibrosis was alleviated by Sp1 in human RTECs by directly modulating Klotho expression, which help to further understand the transcriptional regulation of Klotho in renal disease models.

Indexed as

Kidney TubulesCell LineEpithelial CellsFibrosisGene Expression RegulationGlucuronidaseHEK293 CellsHumansKidney DiseasesKlotho ProteinsSp1 Transcription FactorTransforming Growth Factor beta1GlucuronidaseKlotho ProteinsSP1 protein, humanSp1 Transcription FactorTransforming Growth Factor beta1KlothoRenal tubular epithelial cellsSp1Transcriptional regulation

Identifiers

PMID32571212
PMCPMC7309980
OpenAlexW3036563325

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.