Evidence map›Paper›PMID 35011628›Full record

ArticleCells2021

The Isoquinoline-Sulfonamide Compound H-1337 Attenuates SU5416/Hypoxia-Induced Pulmonary Arterial Hypertension in Rats.

Hiroki Shoji, Yoko Yoshida, Takayuki Jujo Sanada, Akira Naito, Junko Maruyama, Erquan Zhang, Kengo Sumi, Seiichiro Sakao, Kazuo Maruyama, Hiroyoshi Hidaka and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 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
0.7field-weighted citation impact, top 27% 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, 5 citations in OpenAlex.

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

11 authors at 3 institutions in 1 country.

Hiroki ShojiDepartment of Respirology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Yoko YoshidaD. Western Therapeutics Institute, Inc., Nagoya 460-0003, Japan.
Takayuki Jujo SanadaDepartment of Respirology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.ORCID 0000-0001-5725-1810
Akira NaitoDepartment of Respirology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Junko MaruyamaDepartment of Anesthesiology and Critical Care Medicine, School of Medicine, Mie University, Mie 514-8507, Japan.
Erquan ZhangDepartment of Anesthesiology and Critical Care Medicine, School of Medicine, Mie University, Mie 514-8507, Japan.
Kengo SumiD. Western Therapeutics Institute, Inc., Nagoya 460-0003, Japan.
Seiichiro SakaoDepartment of Respirology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Kazuo MaruyamaDepartment of Anesthesiology and Critical Care Medicine, School of Medicine, Mie University, Mie 514-8507, Japan.
Hiroyoshi HidakaD. Western Therapeutics Institute, Inc., Nagoya 460-0003, Japan.
Koichiro TatsumiDepartment of Respirology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Chiba University · JPMie University · JPSuzuka University of Medical Science · JP

Funding

D.Western Therapeutics Institute None.JSPS KAKENHI 17H04181 and 19H03664the Japan Agency for Medical Research and Development 15ek0109127h0001the Ministry of Health, Labour and Welfare, Japan H26-Intractable diseases-General-076
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is characterized by elevated pulmonary arterial pressure and right heart failure. Selective pulmonary vasodilators have improved the prognosis of PAH; however, they are not able to reverse pulmonary vascular remodeling. Therefore, a search for new treatment agents is required. H-1337 is an isoquinoline-sulfonamide compound that inhibits multiple serine/threonine kinases, including Rho-associated protein kinase (ROCK) and mammalian target of rapamycin (mTOR). Here, we investigated the effects of H-1337 on pulmonary hypertension and remodeling in the pulmonary vasculature and right ventricle in experimental PAH induced by SU5416 and hypoxia exposure. H-1337 and H-1337M1 exerted inhibitory effects on ROCK and Akt. H-1337 inhibited the phosphorylation of myosin light chain and mTOR and suppressed the proliferation of smooth muscle cells in vitro. H-1337 treatment also suppressed the phosphorylation of myosin light chain and mTOR in the pulmonary vasculature and decreased right ventricular systolic pressure and the extent of occlusive pulmonary vascular lesions. Furthermore, H-1337 suppressed aggravation of right ventricle hypertrophy. In conclusion, our data demonstrated that inhibition of ROCK and mTOR pathways with H-1337 suppressed the progression of pulmonary vascular remodeling, pulmonary hypertension, and right ventricular remodeling.

Indexed as

AnimalsCell ProliferationHeart VentriclesHumansHypoxiaIndolesIsoquinolinesLungMaleMetabolomeMyosin Light ChainsPhosphorylationProto-Oncogene Proteins c-aktPulmonary Arterial HypertensionPyrrolesRatsIndolesIsoquinolinesMyosin Light ChainsProto-Oncogene Proteins c-aktPyrrolesSemaxinibSulfonamidesTOR Serine-Threonine Kinasesanimal model of pulmonary arterial hypertensionmammalian target of rapamycin signalingpulmonary hypertensionRho-associated protein kinase signalingright ventricular remodeling

Identifiers

PMID35011628
PMCPMC8750965
OpenAlexW4200174937

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.