Evidence map›Paper›PMID 31219801›Full record

ArticleAging2019

TRPM7 channel inhibition exacerbates pulmonary arterial hypertension through MEK/ERK pathway.

Junhui Xing, Mengyu Wang, Jin Hong, Yueqiao Gao, Yuzhou Liu, Heping Gu, Jianzeng Dong, Ling Li

Open access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. AFrontiers in cardiovascular medicine · 2024
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Potential of the TRPM7 channel as a novel therapeutic target for pulmonary arterial hypertension.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2022
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
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  15. Article
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 1 institution in 1 country.

Junhui Xing *Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Mengyu Wang *Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jin Hong *Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yueqiao GaoDepartment of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yuzhou LiuDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Heping GuDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jianzeng DongDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Ling LiDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increased proliferation and apoptosis resistance of pulmonary artery smooth muscle cells (PASMCs) drive the progression of pulmonary arterial hypertension (PAH). The transient receptor potential melastatin 7 (TRPM7) is an endogenous magnesium channel reported to promote the proliferation of SMCs. However, whether TRPM7 is associated with PAH pathogenesis remains uncharacterized. We found that TRPM7 was downregulated in PASMCs from PAH human and Sprague-Dawley rats with hypoxia-induced PAH. Similar results were reproduced in PASMCs treated with PAH stimuli in vitro. Additionally, the TRPM7 currents and intracellular magnesium level in PASMCs were also reduced by PAH stimuli. Functionally, TRPM7 inhibition with waixenicin A or knockdown promoted, and reversely, its overexpression inhibited the proliferation and apoptosis resistance of PASMCs. Moreover, waixenicin A exacerbated hypoxia-induced PAH features in rats. Furthermore, TRPM7 inhibition activated MEK/ERK pathway, and the effects of TRPM7 inhibition were drastically attenuated by pathway specific inhibitor U0126, thus suggesting that activating MEK/ERK pathway is a predominant mechanism through which TRPM7 inhibition exacerbates PAH. In summary, these results may identify TRPM7 as a novel negative regulator in PAH pathogenesis, and suggest that improving its function may represent an antagonistic strategy to modify PAH progression.

Indexed as

AcetatesAnimalsDiterpenesGene Expression RegulationHumansInsulin-Like Growth Factor IInterleukin-6MagnesiumMaleMAP Kinase Signaling SystemProtein Serine-Threonine KinasesPulmonary Arterial HypertensionRatsRats, Sprague-DawleyTRPM Cation ChannelsTumor Necrosis Factor-alphaAcetatesDiterpenesInsulin-Like Growth Factor IInterleukin-6MagnesiumProtein Serine-Threonine KinasesTRPM7 protein, humanTrpm7 protein, ratTRPM Cation ChannelsTumor Necrosis Factor-alphawaixenicin Aapoptosis resistanceproliferationpulmonary arterial hypertensionpulmonary artery smooth muscle cellTRPM7

Identifiers

PMID31219801
PMCPMC6629001
OpenAlexW2953003462

What OpenQuestion holds

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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.