Evidence map›Paper›PMID 33691194›Full record

ArticleTranslational research : the journal of laboratory and clinical medicine2021

Substantial involvement of TRPM7 inhibition in the therapeutic effect of Ophiocordyceps sinensis on pulmonary hypertension.

Keizo Hiraishi, Lin Hai Kurahara, Jianlin Feng, Aya Yamamura, Yuanyuan Cui, Eiji Yahiro, Hiroyasu Yokomise, Tetsuhiko Go, Kaori Ishikawa, Naoya Yokota and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Translational research : the journal of laboratory and clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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
  5. 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

19 authors at 7 institutions in 3 countries.

Keizo HiraishiDepartment of Cardiovascular Physiology, Faculty of Medicine, Kagawa University, Miki-cho, Kita-gun, Kagawa, Japan; Department of Physiology, Fukuoka University School of Medicine, Johnan-ku, Fukuoka, Japan.
Lin Hai KuraharaDepartment of Cardiovascular Physiology, Faculty of Medicine, Kagawa University, Miki-cho, Kita-gun, Kagawa, Japan; Department of Physiology, Fukuoka University School of Medicine, Johnan-ku, Fukuoka, Japan. Electronic address: hailin@med.kagawa-u.ac.jp.
Jianlin FengDepartment of Cell Biology, University of Connecticut Health Center, Farmington, Connecticut.
Aya YamamuraDepartment of Physiology, Aichi Medical University, Nagakute, Aichi, Japan.
Yuanyuan CuiDepartment of Physiology, Fukuoka University School of Medicine, Johnan-ku, Fukuoka, Japan; School of Basic Medical Sciences & Shanxi key Laboratory of Brain Disorders, Xi'an Medical University, Xi'an, China.
Eiji YahiroFukuoka University Medical Education Center, Fukuoka University School of Medicine, Fukuoka University, Johnan-ku, Fukuoka, Japan.
Hiroyasu YokomiseDepartment of General Thoracic Surgery, Faculty of Medicine, Kagawa University, Kita-gun, Miki-cho, Kagawa, Japan.
Tetsuhiko GoDepartment of General Thoracic Surgery, Faculty of Medicine, Kagawa University, Kita-gun, Miki-cho, Kagawa, Japan.
Kaori IshikawaDepartment of General Medicine, Faculty of Medicine, Kagawa University, Kita-gun, Miki-cho, Kagawa, Japan.
Naoya YokotaDepartment of General Thoracic Surgery, Faculty of Medicine, Kagawa University, Kita-gun, Miki-cho, Kagawa, Japan.
Atsushi FujiwaraDepartment of General Thoracic Surgery, Faculty of Medicine, Kagawa University, Kita-gun, Miki-cho, Kagawa, Japan.
Miki OnitsukaDepartment of Pathology, School of Medicine, Fukuoka University, Fukuoka, Japan.
Kohtaro AbeDepartment of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Higashi-ku, Fukuoka, Japan.
Shoji OhgaFaculty of Agriculture, Kyusyu University Professor Emeritus, Kasuya-gun, Fukuoka, Japan.
Toru SatohDivision of Cardiology, Department of Medicine, Kyorin University School of Medicine, Tokyo, Japan.
Yasumasa OkadaDivision of Internal Medicine and Laboratory of Electrophysiology, Murayama Medical Center, Tokyo, Japan.
Lixia YueDepartment of Cell Biology, University of Connecticut Health Center, Farmington, Connecticut.
Ryuji InoueDepartment of Physiology, Fukuoka University School of Medicine, Johnan-ku, Fukuoka, Japan. Electronic address: inouery@fukuoka-u.ac.jp.
Katsuya HiranoDepartment of Cardiovascular Physiology, Faculty of Medicine, Kagawa University, Miki-cho, Kita-gun, Kagawa, Japan.
Fukuoka University · JPKagawa University · JPUConn Health · USAichi Medical University · JPKyorin University · JPKyushu University · JPMurayama Medical Center · JP

Funding

Ca2+ signaling mechanisms in cardiac fibrosisR01HL078960 · NHLBI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YUE, LIXIA · 2005 to 2015
$3.9M
Regulation of TRPM7 ChannelsR01HL147350 · NHLBI · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI RUNNELS, LOREN W, YUE, LIXIA · 2019 to 2022
$2.4M
NHLBI NIH HHS R01 HL078960NHLBI NIH HHS R01 HL147350
6 · The paper itself

Abstract

Ophiocordyceps sinensis (OCS), an entomopathogenic fungus, is known to exert antiproliferative and antitissue remodeling effects. Vascular remodeling and vasoconstriction play critical roles in the development of pulmonary hypertension (PH). The therapeutic potential of OCS for PH was investigated using rodent PH models, and cultured pulmonary artery endothelial and smooth muscle cells (PAECs and PASMCs), with a focus on the involvement of TRPM7. OCS ameliorated the development of PH, right ventricular hypertrophy and dysfunction in the monocrotaline-induced PH rats. The genetic knockout of TRPM7 attenuated the development of PH in mice with monocrotaline pyrrole-induced PH. TRPM7 was associated with medial hypertrophy and the plexiform lesions in rats and humans with PH. OCS suppressed proliferation of PASMCs derived from the PH patients. Ethanol extracts of OCS inhibited TRPM7-like current, TGF-β2-induced endothelial-mesenchymal transition, IL-6-induced STAT3 phosphorylation, and PDGF-induced Akt phosphorylation in PAECs or PASMCs. These inhibitory effects were recapitulated by either siRNA-mediated TRPM7 knockdown or treatment with TRPM7 antagonist FTY-720. OCS and FTY-720 induced vasorelaxation in the isolated normal human pulmonary artery. As a result, the present study proposes the therapeutic potential of OCS for the treatment of PH. The inhibition of TRPM7 is suggested to underlie the therapeutic effect of OCS.

Indexed as

AnimalsCell ProliferationCells, CulturedCordycepsDisease Models, AnimalFingolimod HydrochlorideGene Knockdown TechniquesHumansHypertension, PulmonaryMaleMedicine, Chinese TraditionalMiceMice, KnockoutProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPulmonary ArteryFingolimod HydrochlorideProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSTAT3 Transcription FactorTRPM7 protein, humanTrpm7 protein, mouseTrpm7 protein, ratTRPM Cation Channels

Identifiers

PMID33691194
PMCPMC9225677
OpenAlexW3135634132

What OpenQuestion holds

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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.