Evidence map›Paper›PMID 34240756›Full record

ArticleJournal of clinical laboratory analysis2021

Knockdown of lncRNA MALAT1 ameliorates acute kidney injury by mediating the miR-204/APOL1 pathway.

Hai-Yuan Lu, Guo-Yi Wang, Jin-Wen Zhao, Hai-Tao Jiang

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. LncRNA AK154753 mediates the development of acute kidney ischemia reperfusion injury via the miRZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Article
  7. Article
  8. Article
  9. MALAT1's mJournal of inflammation research · 2025
    Article
  10. Article
  11. Review
  12. LncRNAs in oncogenic microenvironment: from threat to therapy.Frontiers in cell and developmental biology · 2024
    Review
  13. Review
  14. Review
  15. Single-Cell Chromatin and Gene-Regulatory Dynamics of Mouse Nephron Progenitors.Journal of the American Society of Nephrology : JASN · 2022
    Article
  16. 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

4 authors at 2 institutions in 1 country.

Hai-Yuan LuDepartment of Nephrology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Guo-Yi WangDepartment of Nephrology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Jin-Wen ZhaoDepartment of Nephrology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Hai-Tao JiangDepartment of Orthopedics, Huai'an First People's Hospital, Huai'an, China.ORCID https://orcid.org/0000-0003-2129-7344
Xuzhou Medical College · CNHuaian First People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute kidney injury (AKI) was characterized by loss of renal function, associated with chronic kidney disease, end-stage renal disease, and length of hospital stay. Long non-coding RNAs (lncRNAs) participated in AKI development and progression. Here, we aimed to investigate the roles and mechanisms of lncRNA MALAT1 in AKI.

methodsAKI serum samples were obtained from 129 AKI patients. ROC analysis was conducted to confirm the diagnostic value of MALAT1 in differentiating AKI from healthy volunteers. After hypoxic treatment on HK-2 cells, the expressions of inflammatory cytokines, MALAT1, miR-204, APOL1, p65, and p-p65, were measured by RT-qPCR and Western blot assays. The targeted relationship between miR-204 and MALAT1 or miR-204 and APOL1 was determined by luciferase reporter assay and RNA pull-down analysis. After transfection, CCK-8, flow cytometry, and TUNEL staining assays were performed to evaluate the effects of MALAT1 and miR-204 on AKI progression.

resultsFrom the results, lncRNA MALAT1 was strongly elevated in serum samples from AKI patients, with the high sensitivity and specificity concerning differentiating AKI patients from healthy controls. In vitro, we established the AKI cell model after hypoxic treatment. After experiencing hypoxia, we found significantly increased MALAT1, IL-1β, IL-6, and TNF-α expressions along with decreased miR-204 level. Moreover, the targeted relationship between MALAT1 and miR-204 was confirmed. Silencing of MALAT1 could reverse hypoxia-triggered promotion of HK-2 cell apoptosis. Meanwhile, the increase of IL-1β, IL-6, and TNF-α after hypoxia treatment could be repressed by MALAT1 knockdown as well. After co-transfection with MALAT1 silencing and miR-204 inhibition, we found that miR-204 could counteract the effects of MALAT1 on HK-2 cell progression and inflammation after under hypoxic conditions. Finally, NF-κB signaling was inactivated while APOL1 expression was increased in HK-2 cells after hypoxia treatment, and lncRNA MALAT1 inhibition reactivated NF-κB signaling while suppressed APOL1 expression by sponging miR-204.

conclusionsCollectively, these results illustrated that knockdown of lncRNA MALAT1 could ameliorate AKI progression and inflammation by targeting miR-204 through APOL1/NF-κB signaling.

Indexed as

Acute Kidney InjuryAdultApolipoprotein L1Case-Control StudiesCell HypoxiaCell LineFemaleGene Expression RegulationGene Knockdown TechniquesHumansKidney Function TestsMaleMicroRNAsMiddle AgedNF-kappa BRNA, Long NoncodingAPOL1 protein, humanApolipoprotein L1MALAT1 long non-coding RNA, humanMicroRNAsMIRN204 microRNA, humanNF-kappa BRNA, Long Noncodingacute kidney injuryAPOL1inflammationlncRNA MALAT1miR-204

Identifiers

PMID34240756
PMCPMC8373329
OpenAlexW3178714499

What OpenQuestion holds

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LicenceCC BY
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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.