Evidence map›Paper›PMID 22342811›Full record

ReviewVascular pharmacology

Why is coronary collateral growth impaired in type II diabetes and the metabolic syndrome?

Petra Rocic

Open access · greenAbstract readReview
In one paragraph

Review in Vascular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Observational
  7. Coronary remodeling and biomechanics: Are we going with the flow in 2020?American journal of physiology. Heart and circulatory physiology · 2021
    Review
  8. Article
  9. Article
  10. Cardioprotection during ischemia by coronary collateral growth.American journal of physiology. Heart and circulatory physiology · 2019
    Review
  11. Article
  12. Review
  13. Article
  14. Elevated 20-HETE impairs coronary collateral growth in metabolic syndrome via endothelial dysfunction.American journal of physiology. Heart and circulatory physiology · 2017
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Cerebral neovascularization in diabetes: implications for stroke recovery and beyond.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014
    Review
  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

1 author at 1 institution in 1 country.

Petra RocicDepartment of Biochemistry and Molecular Biology, University of South Alabama College of Medicine, Mobile, AL 36688, United States. procic@usouthal.edu
University of South Alabama · US

Funding

Regulation of Coronary Collateral Growth in the Metabolic SyndromeR01HL093052 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI ROCIC, PETRA · 2008 to 2018
$3.7M
NHLBI NIH HHS R01 HL093052
6 · The paper itself

Abstract

Type II diabetes and the metabolic syndrome are strong predictors of severity of occlusive coronary disease and poorer outcomes of coronary revascularization therapies. Coronary collateral growth can provide an alternative or accessory pathway of revascularization. However, collateral growth is impaired in type II diabetes and the metabolic syndrome. Although many factors necessary for collateral growth are known and many interventions have shown promising results in animal studies, not a single attempt to induce coronary collateral growth in human clinical trials has led to satisfactory results. Accordingly, the first part of this review outlines the known deleterious effects of diabetes and the metabolic syndrome on factors necessary for collateral growth, including pro-angiogenic growth factors, endothelial function, the redox state of the coronary circulation, intracellular signaling, leukocytes and bone marrow-derived progenitors cells. The second section highlights the gaps in our current knowledge of how these factors interact with the radically altered environment of the coronary circulation in diabetes and the metabolic syndrome. The interplay between these pathologies and inadequately explored areas related to the temporal regulation of collateral remodeling and the roles of the extracellular matrix, vascular cell phenotype and pro-inflammatory cytokines are emphasized with implications to development of efficient therapies.

Indexed as

AnimalsCollateral CirculationCoronary CirculationCoronary OcclusionCytokinesDiabetes Mellitus, Type 2Extracellular MatrixHumansMetabolic SyndromeSeverity of Illness IndexCytokines

Identifiers

PMID22342811
PMCPMC3359422
OpenAlexW2065370941

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.