Evidence map›Paper›PMID 19754385›Full record

ReviewCurrent pharmaceutical design2009

Rho kinase: an important mediator of atherosclerosis and vascular disease.

Qian Zhou, James K Liao

Open access · greenAbstract readReview
In one paragraph

Review in Current pharmaceutical design, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.2field-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

47 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Direct active Fyn-paxillin interaction regulates vascular smooth muscle cell migration.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2023
    Review
  6. Article
  7. [Rho kinase inhibitors as new local therapy option in primary open angle glaucoma].Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft · 2021
    Review
  8. Article
  9. Article
  10. Role of Macrophages and RhoA Pathway in Atherosclerosis.International journal of molecular sciences · 2020
    Review
  11. Article
  12. Review
  13. KRIT1 Deficiency Promotes Aortic Endothelial Dysfunction.International journal of molecular sciences · 2019
    Article
  14. Review
  15. Review
  16. Article
  17. Tumor necrosis factor-α levels and non-surgical bleeding in continuous-flow left ventricular assist devices.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2018
    Article
  18. Article
  19. In Development-A New Paradigm for Understanding Vascular Disease.Journal of cardiovascular pharmacology · 2017
    Review
  20. 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

2 authors at 1 institution in 1 country.

Qian ZhouVascular Medicine Research Unit, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
James K Liao
Harvard University · US

Funding

TRIGEMINOVASCULAR CONTROL OF CEREBRAL BLOOD VESSELSP50NS010828 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 1985 to 2007
$10.8M
LIPOPROTEINS EFFECTS ON G PROTEIN FUNCTIONR01HL052233 · NHLBI · UNIVERSITY OF CHICAGO · PI LIAO, JAMES KUANG-JAN · 1995 to 2016
$5.3M
Role of PI3-Kinase in Estrogen-induced eNOS ActivationR01DK062729 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI LIAO, JAMES KUANG-JAN · 2003 to 2007
$1.9M
Endothelial Akt in Vascular InjuryR01HL080187 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIAO, JAMES KUANG-JAN · 2006 to 2009
$1.6M
NHLBI NIH HHS HL052233NHLBI NIH HHS HL080187NHLBI NIH HHS R01 HL052233NHLBI NIH HHS R01 HL080187NIDDK NIH HHS R01 DK062729NINDS NIH HHS P50 NS010828
6 · The paper itself

Abstract

Atherosclerosis is a complex inflammatory process characterized by the cross-talk between excessive inflammation and lipid accumulation. In the past few years, compelling evidence suggests that statins can decrease vascular inflammation and attenuate the development of atherosclerosis through their so-called "pleiotropic effects". These cholesterol-independent effects are predominantly due to their ability to inhibit isoprenoid synthesis. In particular, inhibition of geranylgeranylpyrophosphate synthesis leads to inhibition of Rho and its downstream target, Rho-kinase (ROCK). Thus, one of the beneficial effects of statin therapy could be due to inhibitory effects on ROCK. ROCK is involved in mediating diverse cellular functions such as smooth muscle contraction, cell migration and proliferation. While increased ROCK activity is associated with endothelial dysfunction, cerebral ischemia, coronary vasospasms and metabolic syndrome, the inhibition of ROCK by statins or selective ROCK inhibitors leads to up-regulation of endothelial nitric oxide synthase (eNOS), decreased vascular inflammation, and reduced atherosclerotic plaque formation. This review will focus on the impact of ROCK in cardiovascular disease and its contributory role to vascular inflammation and the atherosclerosis.

Indexed as

Signal TransductionAnimalsAnti-Inflammatory AgentsAtherosclerosisHumansHydroxymethylglutaryl-CoA Reductase InhibitorsInflammationLipid MetabolismProtein Kinase Inhibitorsrho-Associated KinasesAnti-Inflammatory AgentsHydroxymethylglutaryl-CoA Reductase InhibitorsProtein Kinase Inhibitorsrho-Associated Kinases

Identifiers

PMID19754385
PMCPMC2896789
OpenAlexW2089750661

What OpenQuestion holds

Texttitle and abstract
LicenceTDM
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.