Evidence map›Paper›PMID 37753070›Full record

ReviewFrontiers in immunology2023

Epigenetic regulation of programmed cell death in hypoxia-induced pulmonary arterial hypertension.

Yuan Jiang, Shasha Song, Jingxin Liu, Liyuan Zhang, Xiaofei Guo, Jiayao Lu, Lie Li, Chao Yang, Qiang Fu, Bin Zeng

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Polygonum cuspidatum Exosome-Like Nanovesicles Alleviate Hypoxic Pulmonary Hypertension by Stabilizing PON1 to Inhibit MAPK-Mediated PASMC Phenotypic Switching.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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

10 authors at 4 institutions in 1 country.

Yuan JiangCollege of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, China.
Shasha SongCollege of Pharmacy, Shenzhen Technology University, Shenzhen, China.
Jingxin LiuCollege of Pharmacy, Shenzhen Technology University, Shenzhen, China.
Liyuan ZhangShanghai Baoxing Biological Equipment Engineering Co., Ltd, Shanghai, China.
Xiaofei GuoNational Engineering Research Center for Marine Aquaculture, Institute of Innovation & Application, Zhejiang Ocean University, Zhoushan, China.
Jiayao LuCollege of Pharmacy, Shenzhen Technology University, Shenzhen, China.
Lie LiShenzhen Reyson Biotechnology Co., Ltd, Shenzhen, China.
Chao YangNational Engineering Research Center for Marine Aquaculture, Institute of Innovation & Application, Zhejiang Ocean University, Zhoushan, China.
Qiang FuCollege of Pharmacy, Shenzhen Technology University, Shenzhen, China.
Bin ZengCollege of Pharmacy, Shenzhen Technology University, Shenzhen, China.
Shenzhen Technology University · CNZhejiang Ocean University · CNBeike Biotechnology (China) · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a severe progressive disease that may cause early right ventricular failure and eventual cardiac failure. The pathogenesis of PAH involves endothelial dysfunction, aberrant proliferation of pulmonary artery smooth muscle cells (PASMCs), and vascular fibrosis. Hypoxia has been shown to induce elevated secretion of vascular endothelial growth factor (VEGF), leading to the development of hypoxic PAH. However, the molecular mechanisms underlying hypoxic PAH remain incompletely understood. Programmed cell death (PCD) is a natural cell death and regulated by certain genes. Emerging evidence suggests that apoptotic resistance contributes to the development of PAH. Moreover, several novel types of PCD, such as autophagy, pyroptosis, and ferroptosis, have been reported to be involved in the development of PAH. Additionally, multiple diverse epigenetic mechanisms including RNA methylation, DNA methylation, histone modification, and the non-coding RNA molecule-mediated processes have been strongly linked to the development of PAH. These epigenetic modifications affect the expression of genes, which produce important changes in cellular biological processes, including PCD. Consequently, a better understanding of the PCD processes and epigenetic modification involved in PAH will provide novel, specific therapeutic strategies for diagnosis and treatment. In this review, we aim to discuss recent advances in epigenetic mechanisms and elucidate the role of epigenetic modifications in regulating PCD in hypoxia-induced PAH.

Indexed as

Heart FailurePulmonary Arterial HypertensionApoptosisEpigenesis, GeneticFamilial Primary Pulmonary HypertensionHumansHypoxiaVascular Endothelial Growth Factor AVascular Endothelial Growth Factor AapoptosisautophagyDNA methylationferroptosishistone modificationnon-coding RNA (ncRNA)pulmonary arterial hypertension (PAH)pyroptosis

Identifiers

PMID37753070
PMCPMC10518698
OpenAlexW4386603264

What OpenQuestion 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 OpenQuestion graph.