Evidence map›Paper›PMID 35813614›Full record

ArticleFrontiers in endocrinology2022

LncRNA MALAT1 Aggravates Renal Tubular Injury

Panai Song, Yinyin Chen, Zhiwen Liu, Hong Liu, Li Xiao, Lin Sun, Jiali Wei, Liyu He

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. 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

8 authors at 5 institutions in 1 country.

Panai SongDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yinyin ChenDepartment of Nephrology, Hunan Provincial People's Hospital, Changsha, China.
Zhiwen LiuDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Hong LiuDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Li XiaoDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Lin SunDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jiali WeiDepartment of Nephrology, Hainan General Hospital, Haiko, China.
Liyu HeDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Soil and Fertilizer Institute of Hunan Province · CNCentral South University · CNHainan General Hospital · CNHunan Provincial People's Hospital · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Diabetic nephropathy (DN) is a serious complication among patients with diabetes. Elucidating its pathogenesis is crucial for identifying novel biomarkers and therapeutic targets for DN. Methods: DN tissues were harvested for examining MALAT1, LIN28A and Nox4. Human kidney-2 (HK-2) cells were treated with high glucose (HG) for establishing a cell model of DN. Cell viability was examined by MTT assay. HG-induced cell apoptosis and secretion of TNF-α and IL-6 were analyzed by TUNEL and ELISA assays, respectively. RIP and RNA pull-down assays were applied to analyze the interaction between MALAT1, LIN28A and Nox4 in HK-2 and human embryonic kidney 293T (HEK-293T) cells. A rat model of DN was established to determine the role of MALAT1 in DN Results: MALAT1, LIN28A and Nox4 were upregulated in DN tissues and HG-treated HK-2 cells. Overexpression of MALAT1, LIN28A or Nox4 reduced cell viability and enhanced cell apoptosis, ROS generation and secretion of inflammatory cytokines in HG-treated HK-2 cells, whereas knockdown of MALAT1, LIN28A or Nox4 exerted opposite effects. Furthermore, MALAT1 directly interacted with LIN28A. Moreover, MALAT1 facilitated the interaction between LIN28A and Nox4 to increase Nox4 stability. Knockdown of Nox4 relieved HG-induced injury by suppressing the AMPK/mTOR signaling in HK-2 cells. Knockdown of MALAT1 alleviated renal tubular epithelial injury by suppressing LIN28A and the Nox4/AMPK/TOR signaling in DN. Conclusion: MALAT1 activates the AMPK/mTOR signaling

Indexed as

Diabetes MellitusDiabetic NephropathiesAMP-Activated Protein KinasesAnimalsCell LineGlucoseHumansKidneyNADPH Oxidase 4RatsRNA-Binding ProteinsRNA, Long NoncodingTOR Serine-Threonine KinasesAMP-Activated Protein KinasesGlucoseLin28A protein, humanLin28A protein, ratMALAT1 long non-coding RNA, humanmTOR protein, ratNADPH Oxidase 4Nox4 protein, ratRNA-Binding ProteinsRNA, Long NoncodingTOR Serine-Threonine KinasesAMPK/mTOR signalingdiabetic nephropathyLIN28AMALAT1renal tubular injury

Identifiers

PMID35813614
PMCPMC9259889
OpenAlexW4283322184

What Socratic 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 Socratic graph.