Evidence map›Paper›PMID 32458165›Full record

ReviewCurrent atherosclerosis reports2020

The Effect of Statins through Mast Cells in the Pathophysiology of Atherosclerosis: a Review.

Hamideh Kouhpeikar, Zahra Delbari, Thozhukat Sathyapalan, Luis E Simental-Mendía, Tannaz Jamialahmadi, Amirhossein Sahebkar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current atherosclerosis reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
3.7field-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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  17. Statins: Beneficial Effects in Treatment of COVID-19.Advances in experimental medicine and biology · 2023
    Article
  18. Review
  19. 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

6 authors at 5 institutions in 3 countries.

Hamideh KouhpeikarDepartment of hematology and blood bank, Tabas school of nursing, Birjand University of Medical Science, Birjand, Iran.
Zahra DelbariInflammation and Inflammatory Diseases Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Thozhukat SathyapalanDepartment of Academic Diabetes, Endocrinology and Metabolism, Hull York Medical School, University of Hull, Hull, HU3 2JZ, UK.
Luis E Simental-MendíaBiomedical Research Unit, Mexican Social Security Institute, Durango, Mexico.
Tannaz JamialahmadiBiotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
Amirhossein SahebkarHalal Research Center of IRI, FDA, Tehran, Iran. sahebkara@mums.ac.ir.
Mashhad University of Medical Sciences · IRMexican Social Security Institute · MXNiroo Research Institute · IRUniversity of Birjand · IRUniversity of Hull · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewIn this review, we discuss the evidence supporting the effects of statins on mast cells (MCs) in atherosclerosis and their molecular mechanism of action. RECENT

findingsStatins or HMG-CoA reductase inhibitors are known for their lipid-lowering properties and are widely used in the prevention and treatment of cardiovascular diseases. There is growing evidence that statins have an inhibitory effect on MCs, which contributes to the pleiotropic effect of statins in various diseases. MCs are one of the crucial effectors of the immune system which play an essential role in the pathogenesis of multiple disorders. Recent studies have shown that MCs are involved in the development of atherosclerotic plaques. MCs secrete various inflammatory cytokines (IL-6, IL4, TNF-α, and IFNγ) and inflammatory mediators (histamine, tryptase, proteoglycans) after activation by various stimulants. This, in turn, will exacerbate atherosclerosis. Statins suppress the activation of MCs via IgE inhibition which leads to inhibition of inflammatory mediators and cytokines which are involved in the development and progression of atherosclerosis. In keeping with this evidence presented here, MCs can be considered as one of the therapeutic targets for statins in the treatment of atherosclerosis.

Indexed as

AnimalsAtherosclerosisCell DegranulationCytokinesHistamine ReleaseHumansHydroxymethylglutaryl-CoA Reductase InhibitorsMast CellsMatrix Metalloproteinase InhibitorsPhospholipase A2 InhibitorsPlaque, AtheroscleroticReceptors, LDLToll-Like ReceptorsCytokinesHydroxymethylglutaryl-CoA Reductase InhibitorsMatrix Metalloproteinase InhibitorsPhospholipase A2 InhibitorsReceptors, LDLToll-Like ReceptorsAtherosclerosisInflammationMast cellsStatin

Identifiers

PMID32458165
OpenAlexW3029697162

What OpenQuestion holds

Texttitle and abstract
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.