Evidence mapPaperPMID 42434640Full record

ReviewCureus2026

A Unifying Model of Inflammatory Amplification: Insights From Colchicine Across Cardiometabolic and Infectious Disease.

Amir B Rabbani

Abstract readReview
In one paragraph

Review in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Amir B RabbaniCardiology, University of California, Los Angeles (UCLA) Health, Los Angeles, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is a shared biological process underlying diseases that are traditionally viewed as distinct, including viral infections, coronary artery disease, and metabolic disorders. Despite differing clinical presentations, these conditions are driven by common immune-inflammatory pathways. This review describes how interactions between the innate and adaptive immune systems can become dysregulated, leading to a self-amplifying inflammatory cycle characterized by persistent immune activation, cytokine signaling, and tissue injury. Within this framework, inflammasome activation and immunometabolic dysfunction emerge as central drivers of disease. The role of colchicine is then examined as a therapeutic model that targets upstream components of the inflammatory amplification cascade. Finally, emerging therapeutic strategies are discussed, along with key gaps that may help guide more targeted approaches to treatment in the future.

Indexed as

atherosclerosiscolchicinecytokine signalinginflammationinnate immunitynlrp3 inflammasome

Identifiers

PMID42434640
PMCPMC13352497

What Socratic holds

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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.