Evidence map›Paper›PMID 18536743›Full record

ReviewBritish journal of pharmacology2008

Therapeutic potential of RhoA/Rho kinase inhibitors in pulmonary hypertension.

M Oka, K A Fagan, P L Jones, I F McMurtry

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
9.5field-weighted citation impact, top 1% 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

78 citing papers in PubMed, 178 citations in OpenAlex.

  1. Review
  2. Review
  3. Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025
    Review
  4. Review
  5. Review
  6. Article
  7. Regulation of myosin light-chain phosphorylation and its roles in cardiovascular physiology and pathophysiology.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Review
  8. Article
  9. Article
  10. Review
  11. Pharmacokinetics of inhaled nanotherapeutics for pulmonary delivery.Journal of controlled release : official journal of the Controlled Release Society · 2020
    Review
  12. Review
  13. Purinergic Dysfunction in Pulmonary Arterial Hypertension.Journal of the American Heart Association · 2020
    Review
  14. Altered Lipid Domains Facilitate Enhanced Pulmonary Vasoconstriction after Chronic Hypoxia.American journal of respiratory cell and molecular biology · 2020
    Article
  15. Article
  16. Review
  17. The Search for Disease-Modifying Therapies in Pulmonary Hypertension.Journal of cardiovascular pharmacology and therapeutics · 2019
    Review
  18. Review
  19. Hypoxia-induced Pulmonary Hypertension in Different Mouse Strains: Relation to Transcriptome.American journal of respiratory cell and molecular biology · 2019
    Article
  20. Article

18 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

M OkaDepartment of Pharmacology and Center for Lung Biology, University of South Alabama, College of Medicine, Mobile, AL 36688, USA. moka@usouthal.edu
K A Fagan
P L Jones
I F McMurtry
University of South Alabama · USUniversity of Pennsylvania · US

Funding

VRAC and Rho in pulmonary EC proliferationP01HL014985 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI STENMARK, KURT R. · 1985 to 2019
$35.1M
Translational Pulmonary Vascular Biology ProgramT32HL007171 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI Sonia Castro Flores, Tim Lahm · 1985 to 2026
$9.4M
NHLBI NIH HHS HL 07171NHLBI NIH HHS HL 14985NHLBI NIH HHS P01 HL014985NHLBI NIH HHS T32 HL007171
6 · The paper itself

Abstract

A burgeoning body of evidence suggests that RhoA/Rho kinase (ROCK) signalling plays an important role in the pathogenesis of various experimental models of pulmonary hypertension (PH), including chronic hypoxia-, monocrotaline-, bleomycin-, shunt- and vascular endothelial growth factor receptor inhibition plus chronic hypoxia-induced PH. ROCK has been incriminated in pathophysiologic events ranging from mediation of sustained abnormal vasoconstriction to promotion of vascular inflammation and remodelling. In addition, the 3-hydroxy-3-methylglutaryl CoA reductase inhibitors, statins, which inhibit activation of RhoA by preventing post-translational isoprenylation of the protein and its translocation to the plasma membrane ameliorate PH in several different rat models, and may also be effective in PH patients. Also, phosphorylation of RhoA and prevention of its translocation to the plasma membrane are involved in the protective effect of the type 5-PDE inhibitor, sildenafil, against hypoxia- and bleomycin-induced PH. Collectively, these and other observations indicate that independent of the cause of PH, activation of the RhoA/ROCK pathway serves as a point of convergence of various signalling cascades in the pathogenesis of the disease. We propose that ROCK inhibitors and other drugs that inhibit this pathway might be useful in the treatment of various forms of PH.

Indexed as

AnimalsDisease Models, AnimalHumansHydroxymethylglutaryl-CoA Reductase InhibitorsHypertension, PulmonaryProtein Kinase InhibitorsrhoA GTP-Binding Proteinrho-Associated KinasesSignal TransductionHydroxymethylglutaryl-CoA Reductase InhibitorsProtein Kinase InhibitorsrhoA GTP-Binding Proteinrho-Associated Kinases

Identifiers

PMID18536743
PMCPMC2579659
OpenAlexW1579639018

What OpenQuestion holds

Textmetadata
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.