Evidence map›Paper›PMID 42795377›Full record

ReviewLife (Basel, Switzerland)2026

Red Blood Cell Distribution Width Is a Biomarker of Red Cell Dysfunction Associated with Inflammation, Macrophage Polarization, and Coronary Artery Calcification: A Prognostic Marker in Cardiovascular Disease and a Potential Target for Anti-Cytokine Therapy.

Kitty Inzunza-Esparza, Artemio García-Escobar

Abstract readReview
In one paragraph

Review in Life (Basel, Switzerland), 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

2 authors.

Kitty Inzunza-EsparzaInstitute for Development and People, Francisco de Vitoria University, M-515, km 1, 800, 28223 Madrid, Spain.
Artemio García-EscobarCardiology Department, Quironsalud University Hospital Madrid, Calle Diego de Velázquez, 1, 28223 Madrid, Spain.ORCID 0000-0002-6786-3498

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronary heart disease represents a great economic expense, especially coronary artery calcification (CAC), which is associated with worse clinical outcomes and increased technical complexity of percutaneous coronary intervention. Red cell distribution width (RDW) is a marker of dysregulated erythropoiesis associated with inflammation and iron accumulation in macrophages that is mediated by hepcidin. Research has indicated that higher RDW levels are linked to an increased risk of adverse cardiovascular events, and some studies have shown an association with CAC. This narrative review aims to summarize the current evidence on the mechanisms responsible for elevated RDW and its relationship with inflammation and CAC. Systemic inflammation induces the expression of hepcidin, which alters iron levels; macrophages, depending on iron levels, can help to resolve inflammation or trigger inflammation in atherosclerotic cardiovascular disease (ASCVD) and can induce vascular calcification. This is known as macrophage polarization. Evidence from large-scale clinical trials has established the involvement of immune-mediated inflammation in the pathogenesis of ASCVD. Thus, systemic inflammation is a novel cardiovascular risk factor that can be treated with anti-cytokine therapy. RDW could be a useful marker of inflammation associated with CAC and a risk marker for experiencing adverse cardiovascular events.

Indexed as

anti-cytokine therapyatherosclerotic cardiovascular diseaseclonal hematopoiesis of indeterminate potentialcoronary artery calcificationferritinhepcidininflammationinterleukin-6macrophage polarizationred blood cell distribution width

Identifiers

PMID42795377
PMCPMC13608391

What OpenQuestion holds

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Registered trials

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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.