Evidence map›Paper›PMID 39936945›Full record

ReviewCells2025

Inflammatory Pathways in Coronary Artery Disease: Which Ones to Target for Secondary Prevention?

Wan-Hei Cheng, Ying Wang

Abstract readReview
In one paragraph

Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Observational
  4. Medical Management of Coronary Artery Disease: An Update.The International journal of angiology : official publication of the International College of Angiology, Inc · 2025
    Review
  5. 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

2 authors.

Wan-Hei ChengDepartment of Pathology and Laboratory Medicine, Faculty of Medicine, University of British Columbia, Vancouver, BC V6T 1Z7, Canada.
Ying WangDepartment of Pathology and Laboratory Medicine, Faculty of Medicine, University of British Columbia, Vancouver, BC V6T 1Z7, Canada.ORCID 0000-0002-1444-5778

Funding

Heart and Stroke Foundation of Canada G-24-0037540
6 · The paper itself

Abstract

Coronary artery disease (CAD), the build-up of atherosclerotic plaques on the wall of blood vessels, causes adverse cardiovascular events. Secondary prevention focuses on treating patients with existing plaques to prevent disease progression. Recent studies have shown that inflammation is an independent risk factor that drives disease progression, and targeting inflammation could be an effective therapeutic strategy for secondary prevention. In this review, we highlighted the roles of several inflammatory pathways in rupture and erosion, two major processes through which established plaques lead to adverse cardiovascular events. In the past 15 years, numerous clinical trials have tested the therapeutic potential of targeting these pathways, including neutralizing inflammatory cytokines and blocking signaling transduction of the inflammatory pathways. Only colchicine was approved for clinical use in patients with CAD. This is primarily due to the multifaceted roles of inflammatory pathways in disease progression. Commonly used pre-clinical models provided robust information for the onset of early disease but limited understanding of the inflammatory network in established plaques. This review will summarize lessons learned from successful and failed clinical trials to advocate for assessing inflammation in established plaques before designing therapeutics for secondary prevention.

Indexed as

Coronary Artery DiseaseInflammationSecondary PreventionAnimalsHumansPlaque, AtheroscleroticSignal Transductioncoronary artery diseaseinflammationsecondary prevention

Identifiers

PMID39936945
PMCPMC11817712

What Socratic holds

Textmetadata
LicenceCC BY
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.