Evidence map›Paper›PMID 21929346›Full record

ReviewFuture cardiology2011

Rho kinase as a therapeutic target in cardiovascular disease.

Michelle Surma, Lei Wei, Jianjian Shi

Open access · greenAbstract readReview
In one paragraph

Review in Future cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 186 citations in OpenAlex.

  1. A Systematic Review of Novel Therapies of Pulmonary Arterial Hypertension.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2024
    Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
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  12. Review
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  14. Article
  15. Article
  16. Article
  17. Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022
    Review
  18. Rho Kinases in Embryonic Development and Stem Cell Research.Archivum immunologiae et therapiae experimentalis · 2022
    Review
  19. Review
  20. Review

23 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

3 authors at 2 institutions in 1 country.

Michelle SurmaRiley Heart Research Centre, Wells Centre for Pediatric Research, Department of Pediatrics, Indiana University, School of Medicine, Indianapolis, IN, USA.
Lei Wei
Jianjian Shi
Indiana University – Purdue University Indianapolis · USRiley Hospital for Children · US

Funding

REGULATION OF CARDIOMYOCYTE SURVIVALP01HL085098 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FIELD, LOREN J · 2007 to 2011
$10.9M
NHLBI NIH HHS P01 HL085098
6 · The paper itself

Abstract

Rho kinase (ROCK) belongs to the AGC (PKA/PKG/PKC) family of serine/threonine kinases and is a major downstream effector of the small GTPase RhoA. ROCK plays central roles in the organization of the actin cytoskeleton and is involved in a wide range of fundamental cellular functions such as contraction, adhesion, migration, proliferation and gene expression. Two ROCK isoforms, ROCK1 and ROCK2, are assumed to be functionally redundant, based largely on the major common activators, the high degree of homology within the kinase domain and studies from overexpression with kinase constructs and chemical inhibitors (e.g., Y27632 and fasudil), which inhibit both ROCK1 and ROCK2. Extensive experimental and clinical studies support a critical role for the RhoA/ROCK pathway in the vascular bed in the pathogenesis of cardiovascular diseases, in which increased ROCK activity mediates vascular smooth muscle cell hypercontraction, endothelial dysfunction, inflammatory cell recruitment and vascular remodeling. Recent experimental studies, using ROCK inhibitors or genetic mouse models, indicate that the RhoA/ROCK pathway in myocardium contributes to cardiac remodeling induced by ischemic injury or persistent hypertrophic stress, thereby leading to cardiac decompensation and heart failure. This article, based on recent molecular, cellular and animal studies, focuses on the current understanding of ROCK signaling in cardiovascular diseases and in the pathogenesis of heart failure.

Indexed as

1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineAmidesApoptosisCardiovascular DiseasesCoronary Artery DiseaseEnzyme InhibitorsFemaleGene Expression Regulation, EnzymologicHeart FailureHumansMaleMyocytes, CardiacProtein IsoformsProtein Kinase InhibitorsPyridinesrho-Associated Kinases1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineAmidesEnzyme InhibitorsfasudilProtein IsoformsProtein Kinase InhibitorsPyridinesrho-Associated KinasesROCK1 protein, humanROCK2 protein, humanY 27632

Identifiers

PMID21929346
PMCPMC3193795
OpenAlexW2052074844

What OpenQuestion holds

Textmetadata
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.