Evidence map›Paper›PMID 19707285›Full record

ReviewVascular health and risk management2009

RhoA/Rho-kinase signaling: a therapeutic target in pulmonary hypertension.

Scott A Barman, Shu Zhu, Richard E White

Open access · goldAbstract readReview
In one paragraph

Review in Vascular health and risk management, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. 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
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Hypoxia-induced Pulmonary Hypertension in Different Mouse Strains: Relation to Transcriptome.American journal of respiratory cell and molecular biology · 2019
    Article
  16. Rho kinase signaling and cardiac physiology.Current opinion in physiology · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Scott A BarmanDepartment of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912, USA. sbarman@mcg.edu
Shu Zhu
Richard E White
Augusta University · US

Funding

PKC Signaling in cAMP-Induced Pulmonary VasodilationR01HL068026 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI BARMAN, SCOTT A · 2001 to 2010
$2.3M
Estrogen dual effects on coronary arteriesR01HL073890 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI WHITE, RICHARD E · 2005 to 2008
$1.3M
NHLBI NIH HHS HL68026NHLBI NIH HHS HL73890NHLBI NIH HHS R01 HL068026NHLBI NIH HHS R01 HL073890
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a devastating disease characterized by progressive elevation of pulmonary arterial pressure and vascular resistance due to pulmonary vasoconstriction and vessel remodeling as well as inflammation. Rho-kinases (ROCKs) are one of the best-described effectors of the small G-protein RhoA, and ROCKs are involved in a variety of cellular functions including muscle cell contraction, proliferation and vascular inflammation through inhibition of myosin light chain phosphatase and activation of downstream mediators. A plethora of evidence in animal models suggests that heightened RhoA/ROCK signaling is important in the pathogenesis of pulmonary hypertension by causing enhanced constriction and remodeling of the pulmonary vasculature. Both animal and clinical studies suggest that ROCK inhibitors are effective for treatment of severe PAH with minimal risk, which supports the premise that ROCKs are important therapeutic targets in pulmonary hypertension and that ROCK inhibitors are a promising new class of drugs for this devastating disease.

Indexed as

AnimalsAntihypertensive AgentsBlood PressureDisease Models, AnimalEvidence-Based MedicineHumansHypertension, PulmonaryMuscle, Smooth, VascularProtein Kinase InhibitorsrhoA GTP-Binding Proteinrho-Associated KinasesSignal TransductionTreatment OutcomeVascular ResistanceVasoconstrictionAntihypertensive AgentsProtein Kinase InhibitorsrhoA GTP-Binding Proteinrho-Associated Kinasesfasudilpulmonary arterial hypertensionRho-kinasevasoconstriction

Identifiers

PMID19707285
PMCPMC2731064
OpenAlexW1999871489

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.