Evidence map›Paper›PMID 33407472›Full record

ArticleRespiratory research2021

Resistin-like molecule β acts as a mitogenic factor in hypoxic pulmonary hypertension via the Ca

Heshen Tian, Lei Liu, Ying Wu, Ruiwen Wang, Yongliang Jiang, Ruicheng Hu, Liming Zhu, Linwei Li, Yanyan Fang, Chulan Yang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.4field-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

29 citing papers in PubMed, 50 citations in OpenAlex.

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  14. Insights into Endothelin Receptors in Pulmonary Hypertension.International journal of molecular sciences · 2023
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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

13 authors at 3 institutions in 1 country.

Heshen TianDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China.
Lei LiuDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China.
Ying WuDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China.
Ruiwen WangDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China.
Yongliang JiangDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China.
Ruicheng HuDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China.
Liming ZhuDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China.
Linwei LiDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China.
Yanyan FangDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China.
Chulan YangDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China.
Lianzhi JiDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China.
Guoyu LiuDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China.
Aiguo DaiDepartment of Respiratory Medicine & Department of Geriatric, Hunan Provincial People's Hospital/The First Affiliated Hospital of Hunan Normal University, Changsha, 410016, Hunan, People's Republic of China. daiaiguo2003@163.com.
Hunan Normal University · CNHunan Provincial People's Hospital · CNHunan University of Traditional Chinese Medicine · CN

Funding

National Natural Science Foundation of China 81270118National Natural Science Foundation of China 81570052
6 · The paper itself

Abstract

backgroundPulmonary arterial smooth muscle cell (PASMC) proliferation plays a crucial role in hypoxia-induced pulmonary hypertension (HPH). Previous studies have found that resistin-like molecule β (RELM-β) is upregulated de novo in response to hypoxia in cultured human PASMCs (hPASMCs). RELM-β has been reported to promote hPASMC proliferation and is involved in pulmonary vascular remodeling in patients with PAH. However, the expression pattern, effects, and mechanisms of action of RELM-β in HPH remain unclear.

methodsWe assessed the expression pattern, mitogenetic effect, and mechanism of action of RELM-β in a rat HPH model and in hPASMCs.

resultsOverexpression of RELM-β caused hemodynamic changes in a rat model of HPH similar to those induced by chronic hypoxia, including increased mean right ventricular systolic pressure (mRVSP), right ventricular hypertrophy index (RVHI) and thickening of small pulmonary arterioles. Knockdown of RELM-β partially blocked the increases in mRVSP, RVHI, and vascular remodeling induced by hypoxia. The phosphorylation levels of the PI3K, Akt, mTOR, PKC, and MAPK proteins were significantly up- or downregulated by RELM-β gene overexpression or silencing, respectively. Recombinant RELM-β protein increased the intracellular Ca

conclusionsOur findings suggest that RELM-β acts as a cytokine-like growth factor in the development of HPH and that the effects of RELM-β are likely to be mediated by the Ca

Indexed as

AnimalsCalciumCells, CulturedGene Knockdown TechniquesGrowth SubstancesHormones, EctopicHypertension, PulmonaryMaleMAP Kinase Signaling SystemPhosphatidylinositol 3-KinasesProtein Kinase CProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyCalciumGrowth SubstancesHormones, EctopicPhosphatidylinositol 3-KinasesProtein Kinase CProto-Oncogene Proteins c-aktRETNLG protein, ratCa2+Hypoxic pulmonary arterial hypertensionPulmonary vascular remodelingResistin-like molecule βSignaling pathwaySOCE

Identifiers

PMID33407472
PMCPMC7789700
OpenAlexW3119104706

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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.