Evidence map›Paper›PMID 20736412›Full record

ReviewPhysiological genomics2010

Vascular smooth muscle phenotypic diversity and function.

Steven A Fisher

Open access · greenAbstract readReview
In one paragraph

Review in Physiological genomics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
4.5field-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

77 citing papers in PubMed, 176 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Smooth muscle contractile cytoskeleton in health and disease.Journal of muscle research and cell motility · 2026
    Review
  5. MBNL loss of function in smooth muscle as a model for myotonic dystrophy associated gastrointestinal dysmotility.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Genetic Insights Into Coronary Microvascular Disease.Microcirculation (New York, N.Y. : 1994) · 2025
    Review
  13. Review
  14. Bioengineering vascularization.Development (Cambridge, England) · 2024
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

17 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

1 author at 1 institution in 1 country.

Steven A FisherDepartment of Medicine, and Cardiovascular Research Institute, Case Western Reserve University, Cleveland, Ohio 44106-7290, USA. Steven.fisher@case.edu
Case Western Reserve University · US

Funding

SMOOTH MUSCLE MYOSIN PHOSPHATASE SUBUNIT ISOFORMSR01HL066171 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI FISHER, STEVEN A. · 2001 to 2013
$3.8M
NHLBI NIH HHS R01 HL-66171
6 · The paper itself

Abstract

The control of force production in vascular smooth muscle is critical to the normal regulation of blood flow and pressure, and altered regulation is common to diseases such as hypertension, heart failure, and ischemia. A great deal has been learned about imbalances in vasoconstrictor and vasodilator signals, e.g., angiotensin, endothelin, norepinephrine, and nitric oxide, that regulate vascular tone in normal and disease contexts. In contrast there has been limited study of how the phenotypic state of the vascular smooth muscle cell may influence the contractile response to these signaling pathways dependent upon the developmental, tissue-specific (vascular bed) or disease context. Smooth, skeletal, and cardiac muscle lineages are traditionally classified into fast or slow sublineages based on rates of contraction and relaxation, recognizing that this simple dichotomy vastly underrepresents muscle phenotypic diversity. A great deal has been learned about developmental specification of the striated muscle sublineages and their phenotypic interconversions in the mature animal under the control of mechanical load, neural input, and hormones. In contrast there has been relatively limited study of smooth muscle contractile phenotypic diversity. This is surprising given the number of diseases in which smooth muscle contractile dysfunction plays a key role. This review focuses on smooth muscle contractile phenotypic diversity in the vascular system, how it is generated, and how it may determine vascular function in developmental and disease contexts.

Indexed as

AnimalsBlood VesselsHemodynamicsHumansHypertensionModels, BiologicalMuscle ContractionMuscle, Smooth, VascularNeuromuscular DiseasesSignal Transduction

Identifiers

PMID20736412
PMCPMC3008361
OpenAlexW1975244725

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.