In one paragraphArticle in Biomolecules, 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
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
12 authors.
Cristina EspadasLaboratory of Vascular Pathology and Diabetes, Fundación Instituto de Investigaciones Sanitarias-Fundación Jiménez Díaz, Universidad Autónoma, 28040 Madrid, Spain.
Manuel Soto-CatalánLaboratory of Vascular Pathology and Diabetes, Fundación Instituto de Investigaciones Sanitarias-Fundación Jiménez Díaz, Universidad Autónoma, 28040 Madrid, Spain.
María Romero-CoteLaboratory of Vascular Pathology and Diabetes, Fundación Instituto de Investigaciones Sanitarias-Fundación Jiménez Díaz, Universidad Autónoma, 28040 Madrid, Spain.ORCID 0009-0006-9639-2281 María KavanaghLaboratory of Vascular Pathology and Diabetes, Fundación Instituto de Investigaciones Sanitarias-Fundación Jiménez Díaz, Universidad Autónoma, 28040 Madrid, Spain.
Isabel Herrero-Del RealLaboratory of Vascular Pathology and Diabetes, Fundación Instituto de Investigaciones Sanitarias-Fundación Jiménez Díaz, Universidad Autónoma, 28040 Madrid, Spain.ORCID 0009-0009-5084-2349 Adriana Ortega-HernándezLaboratory of Vascular Biology and Microbiota, Instituto de Investigaciones Sanitarias Hospital Clínico San Carlos, 28040 Madrid, Spain.ORCID 0009-0006-1426-6194 Jairo Lumpuy-CastilloLaboratory of Vascular Pathology and Diabetes, Fundación Instituto de Investigaciones Sanitarias-Fundación Jiménez Díaz, Universidad Autónoma, 28040 Madrid, Spain.ORCID 0000-0002-3458-0328 Dulcenombre Gómez-GarreLaboratory of Vascular Biology and Microbiota, Instituto de Investigaciones Sanitarias Hospital Clínico San Carlos, 28040 Madrid, Spain.ORCID 0000-0002-5056-6489 Jesús EgidoLaboratory of Vascular Pathology and Diabetes, Fundación Instituto de Investigaciones Sanitarias-Fundación Jiménez Díaz, Universidad Autónoma, 28040 Madrid, Spain.ORCID 0000-0001-6321-2666 José TuñónDepartment of Cardiology, Hospital Fundación Jiménez Díaz, Universidad Autónoma, 28040 Madrid, Spain.ORCID 0000-0002-1373-0999 Carmen Gómez-GuerreroLaboratory of Vascular Pathology and Diabetes, Fundación Instituto de Investigaciones Sanitarias-Fundación Jiménez Díaz, Universidad Autónoma, 28040 Madrid, Spain.ORCID 0000-0001-9001-5414 Óscar LorenzoLaboratory of Vascular Pathology and Diabetes, Fundación Instituto de Investigaciones Sanitarias-Fundación Jiménez Díaz, Universidad Autónoma, 28040 Madrid, Spain.ORCID 0000-0001-5515-6078 Funding
Instituto de Salud Carlos III PI020/00923; PI024/00978
6 · The paper itselfAbstract
backgroundProprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) has been implicated in vascular inflammation beyond its action on LDL-C degradation. We investigated whether PCSK9 may exacerbate proinflammatory signaling of M1 macrophages and if its neutralization with alirocumab could attenuate this effect and plaque progression by LDL-C independent mechanisms.
methodsApoE
resultsAlirocumab reduced plaque lesion (0.42-fold;
conclusionsPCSK9 may be released in parallel to proinflammatory factors such as hsCRP and FGF-23 in patients with ACS, independently of LDL-C levels. PCSK9 may directly promote macrophage-driven inflammatory responses through the TLR4-NFκB-NLRP3 signaling, but its neutralization with alirocumab attenuated this inflammatory axis and limited atherosclerotic progression, supporting an anti-inflammatory benefit secondary to PCSK9 inhibition.
Indexed as
Antibodies, Monoclonal, HumanizedInflammationMacrophagesPlaque, AtheroscleroticProprotein Convertase 9AnimalsCytokinesFemaleHumansMaleMiceMice, KnockoutSignal TransductionToll-Like Receptor 4alirocumabAntibodies, Monoclonal, HumanizedCytokinesPCSK9 protein, humanPcsk9 protein, mouseProprotein Convertase 9Toll-Like Receptor 4alirocumabinflammationNFκBNLRP3PCSK9
Identifiers
PMID41897333
PMCPMC13023508
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