Evidence map›Paper›PMID 33546692›Full record

ArticleJournal of inflammation (London, England)2021

Overexpression of SP1 restores autophagy to alleviate acute renal injury induced by ischemia-reperfusion through the miR-205/PTEN/Akt pathway.

Chong Huang, Yan Chen, Bin Lai, Yan-Xia Chen, Cheng-Yun Xu, Yuan-Fei Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation (London, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Anoikis: To Die or Not to Die?International journal of molecular sciences · 2026
    Review
  2. Molecular mechanisms attributed to colistin renal proximal tubular epithelial cytotoxicity.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. m6A demethylase FTO transcriptionally activated by SP1 improves ischemia reperfusion-triggered acute kidney injury by activating Ambra1/ULK1-mediated autophagy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  8. Review
  9. Article
  10. A protein encoded by circular ZNF609 RNA induces acute kidney injury by activating the AKT/mTOR-autophagy pathway.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  11. Article
  12. 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

6 authors at 1 institution in 1 country.

Chong HuangDepartment of Nephrology, The Second Affiliated Hospital of Nanchang University, 330006, Nanchang, Jiangxi Province, People's Republic of China.
Yan ChenDepartment of Nephrology, The Second Affiliated Hospital of Nanchang University, 330006, Nanchang, Jiangxi Province, People's Republic of China.
Bin LaiDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital of Nanchang University, 330006, Nanchang, Jiangxi Province, People's Republic of China.
Yan-Xia ChenDepartment of Nephrology, The Second Affiliated Hospital of Nanchang University, 330006, Nanchang, Jiangxi Province, People's Republic of China.
Cheng-Yun XuDepartment of Nephrology, The Second Affiliated Hospital of Nanchang University, 330006, Nanchang, Jiangxi Province, People's Republic of China.
Yuan-Fei LiuDepartment of Emergency, The Second Affiliated Hospital of Nanchang University, No.1, Minde Road, 330006, Nanchang, Jiangxi Province, People's Republic of China. yuafee789@163.com.ORCID http://orcid.org/0000-0003-0639-0276
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute kidney injury (AKI) is a major kidney disease with poor clinical outcome. SP1, a well-known transcription factor, plays a critical role in AKI and subsequent kidney repair through the regulation of various cell biologic processes. However, the underlying mechanism of SP1 in these pathological processes remain largely unknown.

methodsAn in vitro HK-2 cells with anoxia-reoxygenation injury model (In vitro simulated ischemic injury disease) and an in vivo rat renal ischemia-reperfusion injury model were used in this study. The expression levels of SP1, miR-205 and PTEN were detected by RT-qPCR, and the protein expression levels of SP1, p62, PTEN, AKT, p-AKT, LC3II, LC3I and Beclin-1 were assayed by western blot. Cell proliferation was assessed by MTT assay, and the cell apoptosis was detected by flow cytometry. The secretions of IL-6 and TNF-α were detected by ELISA. The targeted relationship between miR-205 and PTEN was confirmed by dual luciferase report assay. The expression and positioning of LC-3 were observed by immunofluorescence staining. TUNEL staining was used to detect cell apoptosis and immunohistochemical analysis was used to evaluate the expression of SP1 in renal tissue after ischemia-reperfusion injury in rats.

resultsThe expression of PTEN was upregulated while SP1 and miR-205 were downregulated in renal ischemia-reperfusion injury. Overexpression of SP1 protected renal tubule cell against injury induced by ischemia-reperfusion via miR-205/PTEN/Akt pathway mediated autophagy. Overexpression of SP1 attenuated renal ischemia-reperfusion injury in rats.

conclusionsSP1 overexpression restored autophagy to alleviate acute renal injury induced by ischemia-reperfusion through the miR-205/PTEN/Akt pathway.

Indexed as

AutophagyIschemia/reperfusion injurymiR-205PTENSP1

Identifiers

PMID33546692
PMCPMC7863508
OpenAlexW3128618263

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.