Evidence map›Paper›PMID 41654637›Full record

ArticleScientific reports2026

Increased atherosclerosis and expression of inflammarafts in macrophage foam cells in AIBP-deficient mice.

Shenglin Li, Nicolaus Nazarenkov, Elena Alekseeva, Soo-Ho Choi, Juliana Maria Navia-Pelaez, Aakash Patel, Patrick Secrest, Philip L S M Gordts, Sven Heinz, Yury I Miller

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In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Shenglin LiDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA.
Nicolaus NazarenkovDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA.
Elena AlekseevaDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA.
Soo-Ho ChoiDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA.
Juliana Maria Navia-PelaezDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA.
Aakash PatelDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA.
Patrick SecrestDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA.
Philip L S M GordtsDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA.
Sven HeinzDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA.
Yury I MillerDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA. yumiller@ucsd.edu.

Funding

NIH HHS DK126848NIH HHS HL171505
6 · The paper itself

Abstract

Atherosclerotic lesions comprise different populations of macrophages, including lipid-laden macrophage foam cells and non-foamy, inflammatory macrophages, which play distinct roles in disease progression. Non-foamy macrophages express higher levels of inflammarafts – enlarged, cholesterol-rich lipid rafts hosting assemblies of inflammatory receptors – compared to foam cells in atherosclerotic lesions of Ldlr−/− mice. Apolipoprotein A-I binding protein (AIBP) has been shown to control lipid raft dynamics. This study investigated the effect of systemic AIBP deficiency on inflammaraft expression in foam cells and non-foamy macrophages in atherosclerotic lesions of hypercholesterolemic mice. A larger number of foam cells, with increased neutral lipid accumulation, populated atherosclerotic lesions in Apoa1bp−/−Ldlr−/− mice compared to Ldlr−/− mice. Importantly, AIBP-deficient foam cells expressed higher levels of TLR4 dimers and lipid rafts (markers of inflammarafts) than control mice, accompanied by larger atherosclerotic lesions and larger necrotic cores compared to Ldlr−/− mice. In a model of foam cells, Apoa1bp−/− bone marrow-derived macrophages incubated with oxidized LDL had increased expression of inflammation and atherosclerosis related genes. These results indicate that AIBP deficiency results in a phenotype shift in foam cells, characterized by increased lipid accumulation and increased expression of inflammarafts, and it correlates with the development of advanced atherosclerotic plaques.

Indexed as

AtherosclerosisFoam CellsInflammationAnimalsLipoproteins, LDLMacrophagesMaleMembrane MicrodomainsMiceMice, KnockoutReceptors, LDLToll-Like Receptor 4Lipoproteins, LDLReceptors, LDLToll-Like Receptor 4AIBPAtherosclerosisInflammaraftsLipid raftsMacrophage foam cellTLR4

Identifiers

PMID41654637
PMCPMC12936166

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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.