Evidence map›Paper›PMID 38635022›Full record

ArticleApoptosis : an international journal on programmed cell death2024

LncRNA MIR210HG promotes phenotype switching of pulmonary arterial smooth muscle cells through autophagy-dependent ferroptosis pathway.

Enze Wang, Binbin Zhang, Ling Huang, Pulin Li, Rui Han, Sijing Zhou, Daxiong Zeng, Ran Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
5.7field-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

13 citing papers in PubMed, 20 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Enze Wang *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China.
Binbin Zhang *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China.
Ling Huang *Department of Infectious Diseases, Hefei Second People's Hospital, Hefei, 230001, China.
Pulin LiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China.
Rui HanDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China.
Sijing ZhouDepartment of Occupational Disease, Hefei Third Clinical College of Anhui Medical University, Hefei, 230022, China. zhousijing@yeah.net.
Daxiong ZengDepartment of Pulmonary and Critical Care Medicine, Dushu Lake Hospital, Affiliated to Soochow University, Medical Center of Soochow University, Suzhou, 215006, China. zengdxsz@126.com.
Ran WangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China. wangran@ahmu.edu.cn.
Anhui Medical University · CNFirst Affiliated Hospital of Anhui Medical University · CNFirst Affiliated Hospital of Soochow University · CN

Funding

National Natural Science Foundation of China,China No.81970051
6 · The paper itself

Abstract

Hypoxic pulmonary hypertension (HPH) is a pathophysiological syndrome in which pulmonary vascular pressure increases under hypoxic stimulation and there is an urgent need to develop emerging therapies for the treatment of HPH. LncRNA MIR210HG is a long non-coding RNA closely related to hypoxia and has been widely reported in a variety of tumor diseases. But its mechanism in hypoxic pulmonary hypertension is not clear. In this study, we identified for the first time the potential effect of MIR210HG on disease progression in HPH. Furthermore, we investigated the underlying mechanism through which elevated levels of MIR210HG promotes the transition from a contractile phenotype to a synthetic phenotype in PASMCs under hypoxia via activation of autophagy-dependent ferroptosis pathway. While overexpression of HIF-2α in PASMCs under hypoxia significantly reversed the phenotypic changes induced by MIR210HG knockdown. We further investigated the potential positive regulatory relationship between STAT3 and the transcription of MIR210HG in PASMCs under hypoxic conditions. In addition, we established both in vivo and in vitro models of HPH to validate the differential expression of specific markers associated with hypoxia. Our findings suggest a potential mechanism of LncRNA MIR210HG in the progression of HPH and offer potential targets for disease intervention and treatment.

Indexed as

AutophagyFerroptosisMyocytes, Smooth MusclePhenotypePulmonary ArteryRNA, Long NoncodingAnimalsBasic Helix-Loop-Helix ProteinsCell HypoxiaEndothelial PAS Domain-Containing Protein 1HumansHypertension, PulmonaryHypoxiaMaleMiceRatsBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1RNA, Long NoncodingSTAT3 Transcription FactorAutophagyFerroptosisHypoxic pulmonary hypertensionMIR210HGPhenotype switching

Identifiers

PMID38635022
OpenAlexW4394914671

What OpenQuestion holds

Textmetadata
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.