Evidence map›Paper›PMID 31604167›Full record

ArticleMolecular therapy. Nucleic acids2019

Silencing of lncRNA MALAT1 Prevents Inflammatory Injury after Lung Transplant Ischemia-Reperfusion by Downregulation of IL-8 via p300.

Li Wei, Jiwei Li, Zhijun Han, Zhong Chen, Quan Zhang

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 105 citations in OpenAlex.

  1. Immune Biomarkers of Islet Transplant Rejection Revealed by Synthetic Immunological Niche.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  8. Long non-coding RNAMolecular therapy. Nucleic acids · 2025
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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

5 authors at 2 institutions in 1 country.

Li WeiDepartment of Thoracic Surgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University and People's Hospital of Henan University, Zhengzhou 450003, P.R. China.
Jiwei LiDepartment of Thoracic Surgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University and People's Hospital of Henan University, Zhengzhou 450003, P.R. China. Electronic address: facefuture00114321@163.com.
Zhijun HanDepartment of Thoracic Surgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University and People's Hospital of Henan University, Zhengzhou 450003, P.R. China.
Zhong ChenDepartment of Thoracic Surgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University and People's Hospital of Henan University, Zhengzhou 450003, P.R. China.
Quan ZhangDepartment of Thoracic Surgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University and People's Hospital of Henan University, Zhengzhou 450003, P.R. China.
Henan Provincial People's Hospital · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia-reperfusion injury is a common early complication after lung transplantation. It was reported that long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in ischemia-reperfusion injury and regulates inflammation. This study aimed to explore the role of MALAT1 in inflammatory injury following lung transplant ischemia-reperfusion (LTIR). A LTIR rat model was successfully established, with the expression of MALAT1 and interleukin-8 (IL-8) in lung tissues detected. Then, in vitro loss- and gain-of-function investigations were conducted to evaluate the effect of MALAT1 on pulmonary epithelial cell apoptosis and IL-8 expression. The relationship among MALAT1, p300, and IL-8 was tested. Moreover, a sh-MALAT1-mediated model of LTIR was established in vivo to examine inflammatory injury and chemotaxis infiltration. Both IL-8 and MALAT1 were highly expressed in LTIR. MALAT1 interacted with p300 to regulate the IL-8 expression by recruiting p300. Importantly, silencing of MALAT1 inhibited the chemotaxis of neutrophils by downregulating IL-8 expression via binding to p300. Besides, MALAT1 silencing alleviated the inflammatory injury after LTIR by downregulating IL-8 and inhibiting infiltration and activation of neutrophils. Collectively, these results demonstrated that silencing of MALAT1 ameliorated the inflammatory injury after LTIR by inhibiting chemotaxis of neutrophils through p300-mediated downregulation of IL-8, providing clinical insight for LTIR injury.

Indexed as

chemotaxis of neutrophilsH3K27 acetylationinflammatory injuryinterleukin-8long non-coding RNAlung transplant ischemia-reperfusionmetastasis-associated lung adenocarcinoma transcript 1p300pulmonary epithelial cells

Identifiers

PMID31604167
PMCPMC6796730
OpenAlexW2947604831

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.