Evidence map›Paper›PMID 35944979›Full record

ReviewJournal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi2022

Potential of the TRPM7 channel as a novel therapeutic target for pulmonary arterial hypertension.

Keizo Hiraishi, Lin Hai Kurahara, Kaori Ishikawa, Tetsuhiko Go, Naoya Yokota, Yaopeng Hu, Takayuki Fujita, Ryuji Inoue, Katsuya Hirano

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. The Dysfunction of CaInternational journal of molecular sciences · 2023
    Review
  3. Review
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

9 authors at 2 institutions in 1 country.

Keizo HiraishiDepartment of Cardiovascular Physiology, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan.
Lin Hai KuraharaDepartment of Cardiovascular Physiology, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan.
Kaori IshikawaDepartment of General Medicine, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan.
Tetsuhiko GoDepartment of General Thoracic Surgery, Faculty of Medicine, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan.
Naoya YokotaDepartment of General Thoracic Surgery, Faculty of Medicine, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan.
Yaopeng HuDepartment of Physiology, School of Medicine, Fukuoka University, 8-19-1 Nanakuma, Jounan-ku, Fukuoka-shi, Fukuoka 814-0180, Japan.
Takayuki FujitaDepartment of Physiology, School of Medicine, Fukuoka University, 8-19-1 Nanakuma, Jounan-ku, Fukuoka-shi, Fukuoka 814-0180, Japan.
Ryuji InoueDepartment of Physiology, School of Medicine, Fukuoka University, 8-19-1 Nanakuma, Jounan-ku, Fukuoka-shi, Fukuoka 814-0180, Japan.
Katsuya HiranoDepartment of Cardiovascular Physiology, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan.
Kagawa University · JPFukuoka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is an intractable vascular disease characterized by a progressive increase in pulmonary vascular resistance caused by pulmonary vascular remodeling, which ultimately leads to right-sided heart failure. PAH remains incurable, despite the development of PAH-targeted therapeutics centered on pulmonary artery relaxants. It is necessary to identify the target molecules that contribute to pulmonary artery remodeling. Transient receptor potential (TRP) channels have been suggested to modulate pulmonary artery remodeling. Our study focused on the transient receptor potential ion channel subfamily M, member 7, or the TRPM7 channel, which modulates endothelial-to-mesenchymal transition and smooth muscle proliferation in the pulmonary artery. In this review, we summarize the role and expression profile of TRPM7 channels in PAH progression and discuss TRPM7 channels as possible therapeutic targets. In addition, we discuss the therapeutic effect of a Chinese herbal medicine, Ophiocordyceps sinensis (OCS), on PAH progression, which partly involves TRPM7 inhibition.

Indexed as

Hypertension, PulmonaryPulmonary Arterial HypertensionTransient Receptor Potential ChannelsTRPM Cation ChannelsCell ProliferationFamilial Primary Pulmonary HypertensionHumansMyocytes, Smooth MuscleProtein Serine-Threonine KinasesPulmonary ArteryVascular RemodelingProtein Serine-Threonine KinasesTransient Receptor Potential ChannelsTRPM7 protein, humanTRPM Cation Channelscardiovascular remodelingpulmonary arterial hypertensionTRPM7

Identifiers

PMID35944979
PMCPMC9364263
OpenAlexW4291020813

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.