Evidence map›Paper›PMID 32323759›Full record

ArticleMolecular medicine reports2020

Long non‑coding RNA MALAT1 promotes high glucose‑induced rat cartilage endplate cell apoptosis via the p38/MAPK signalling pathway.

Zengxin Jiang, Qingmin Zeng, Defang Li, Lei Ding, Wei Lu, Mengxuan Bian, Jingping Wu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. PI3KCD gene expression and its role in diabetic intervertebral disc degeneration running title: PI3KCD gene crucial for diabetic IDH.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. The effect of diabetes mellitus on lumbar disc degeneration: an MRI-based study.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2024
    Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Role of non‑coding RNAs in cartilage endplate (Review).Experimental and therapeutic medicine · 2023
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
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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

7 authors at 2 institutions in 1 country.

Zengxin JiangDepartment of Orthopedic Surgery, Fudan University Jinshan Hospital, Shanghai 201508, P.R. China.
Qingmin ZengDepartment of Orthopedic Surgery, Fudan University Jinshan Hospital, Shanghai 201508, P.R. China.
Defang LiDepartment of Orthopedic Surgery, Fudan University Jinshan Hospital, Shanghai 201508, P.R. China.
Lei DingDepartment of Orthopedic Surgery, Fudan University Jinshan Hospital, Shanghai 201508, P.R. China.
Wei LuDepartment of Orthopedic Surgery, Shanghai TCM‑Integrated Hospital, Shanghai University of TCM, Shanghai 200082, P.R. China.
Mengxuan BianDepartment of Orthopedic Surgery, Fudan University Jinshan Hospital, Shanghai 201508, P.R. China.
Jingping WuDepartment of Orthopedic Surgery, Fudan University Jinshan Hospital, Shanghai 201508, P.R. China.
Jinshan Hospital of Fudan University · CNShanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus (DM) contributes to intervertebral disc degeneration (IDD). The long non‑coding RNA MALAT1 has been revealed to play an important role in diabetes‑associated complications. However, the specific role of MALAT1 in diabetes‑associated IDD has not been determined. The aim of the present study was to evaluate the roles of MALAT1 in the apoptosis of cartilage endplate (CEP) cells induced by high glucose and to explore the mechanisms underlying this effect. Rat CEP cells were cultured in high‑glucose medium (25 mM glucose) for 24 or 72 h. Cells cultured in medium containing 5 mM glucose were used as a control. Flow cytometry was used to detect the degree of apoptosis. Reverse transcription‑quantitative PCR was used to measure the expression of MALAT1 mRNA. In addition, CEP cells were treated with different conditions (high glucose, high glucose + MALAT1 negative control, high glucose + MALAT1 RNAi, normal control) for 72 h. Flow cytometry was subsequently used to detect apoptosis and western blotting was used to measure the expression levels of total and phosphorylated p38. The results revealed that high glucose concentration promoted apoptosis and enhanced expression of MALAT1 in CEP cells. Furthermore, MALAT1 knockout decreased the expression levels of total and phosphorylated p38 and reduced the apoptosis of rat CEP cells. The results obtained in the present study indicated that MALAT1 may serve as an important therapeutic target for curing or delaying IDD in patients with diabetes.

Indexed as

AnimalsApoptosisCartilageCells, CulturedChondrocytesFlow CytometryGene Knockout TechniquesGlucoseIntervertebral Disc DegenerationMaleMAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesRatsRats, Sprague-DawleyRNA InterferenceRNA, Long NoncodingGlucoseMALAT1 long noncoding RNA, ratp38 Mitogen-Activated Protein KinasesRNA, Long Noncodingcartilage endplate cell apoptosisdiabetes mellitusintervertebral disc degenerationMALAT1p38/MAPK signalling pathway

Identifiers

PMID32323759
PMCPMC7115198
OpenAlexW3009170351

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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.