Evidence map›Paper›PMID 40111634›Full record

ReviewCurrent atherosclerosis reports2025

Insight into the Mechanistic role of Colchicine in Atherosclerosis.

Hayder M Al-Kuraishy, Ghassan M Sulaiman, Hamdoon A Mohammed, Retaj A Dawood, Ali K Albuhadily, Ali I Al-Gareeb, Daniel J Klionsky, Mosleh M Abomughaid

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current atherosclerosis reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

8 authors.

Hayder M Al-KuraishyDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Ghassan M SulaimanDivision of Biotechnology, Department of Applied Sciences, University of Technology, Baghdad, Iraq. ghassan.m.sulaiman@uotechnology.edu.iq.
Hamdoon A MohammedDepartment of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, Qassim University, 51452, Qassim, Saudi Arabia.
Retaj A DawoodDepartment of Biology, College of Science, Al-Mustaqbal University, Hilla, 51001, Iraq.
Ali K AlbuhadilyDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Ali I Al-GareebJabir Ibn Hayyan Medical University, Al-Ameer Qu, PO.Box13 Kufa, Najaf, Iraq.
Daniel J KlionskyLife Sciences Institute, University of Michigan, Ann Arbor, MI, 48109, USA. klionsky@umich.edu.
Mosleh M AbomughaidDepartment of Medical Laboratory Sciences, College of Applied Medical Sciences, University of Bisha, 255, 67714, Bisha, Saudi Arabia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewGlobally, the prevalence of atherosclerosis (AS) is rising. Currently, there is no specific drug for AS. Therefore, this review aims to discuss the protective mechanisms of colchicine against the development and progression of atherosclerosis (AS). RECENT

findingsMany studies highlighted that the anti-inflammatory drug colchicine reduces the severity of AS, although the underlying mechanism for the beneficial effect of colchicine was not fully clarified. AS is a chronic progressive vascular disorder characterized by the formation of atherosclerotic plaques. Endothelial dysfunction is an initial stage in the pathogenesis of AS that is induced by oxidized low-density lipoprotein (oxLDL). Engulfment of oxLDL by macrophages triggers the development of inflammation due to the release of pro-inflammatory cytokines and growth factors. Inflammatory and adhesion molecules are involved in the pathogenesis of AS. Infiltration and accumulation of leukocytes provoke erosion, rupture, and thrombosis of the atherosclerotic plaque. Therefore, targeting inflammation and leukocyte infiltration by anti-inflammatory agents may reduce AS progression and complications. The anti-inflammatory drug colchicine reduces the severity of AS, although the underlying mechanism for the beneficial effect of colchicine was not fully elucidated. IN

conclusioncolchicine through inhibition of vascular inflammation, oxidative stress, platelet aggregation and the modulation of autophagy reduces the development and progression of AS.

Indexed as

Anti-Inflammatory AgentsAtherosclerosisColchicineHumansInflammationOxidative StressAnti-Inflammatory AgentsColchicineAtherosclerosisAutophagyColchicineEndothelial dysfunctionInflammatory moleculesOxidative stressPathogenesis

Identifiers

PMID40111634

What Socratic 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 Socratic graph.