Evidence map›Paper›PMID 40931837›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2025

Single-Cell Analysis Reveals a Critical Role for Macrophage Epsins in Regulating the Origin of Foam Cells in Atherosclerosis.

Kulandaisamy Arulsamy, Kui Cui, Bo Zhu, Beibei Wang, Shahram Eisa-Beygi, Anna Voronova, Xinlei Gao, Krishan Gupta, Lili Zhang, Kaifu Chen and 1 more

Abstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 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. Review
  3. Review
  4. Review
  5. Review
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

11 authors.

Kulandaisamy Arulsamy *Basic and Translational Research Division, Department of Cardiology, Boston Children's Hospital, MA (K.A., X.G., K.G., L.Z., K. Chen).ORCID 0000-0002-3367-2669
Kui Cui *Vascular Biology Program, Boston Children's Hospital and Harvard Medical School, MA (K. Cui, B.Z., B.W., S.E.-B., A.V., H.C.).ORCID 0000-0003-2615-4932
Bo ZhuVascular Biology Program, Boston Children's Hospital and Harvard Medical School, MA (K. Cui, B.Z., B.W., S.E.-B., A.V., H.C.).ORCID 0000-0002-8962-1094
Beibei WangVascular Biology Program, Boston Children's Hospital and Harvard Medical School, MA (K. Cui, B.Z., B.W., S.E.-B., A.V., H.C.).ORCID 0009-0009-8359-2518
Shahram Eisa-BeygiVascular Biology Program, Boston Children's Hospital and Harvard Medical School, MA (K. Cui, B.Z., B.W., S.E.-B., A.V., H.C.).
Anna VoronovaVascular Biology Program, Boston Children's Hospital and Harvard Medical School, MA (K. Cui, B.Z., B.W., S.E.-B., A.V., H.C.).
Xinlei GaoBasic and Translational Research Division, Department of Cardiology, Boston Children's Hospital, MA (K.A., X.G., K.G., L.Z., K. Chen).
Krishan GuptaBasic and Translational Research Division, Department of Cardiology, Boston Children's Hospital, MA (K.A., X.G., K.G., L.Z., K. Chen).ORCID 0000-0002-3390-9494
Lili ZhangBasic and Translational Research Division, Department of Cardiology, Boston Children's Hospital, MA (K.A., X.G., K.G., L.Z., K. Chen).ORCID 0000-0002-5032-7031
Kaifu ChenBasic and Translational Research Division, Department of Cardiology, Boston Children's Hospital, MA (K.A., X.G., K.G., L.Z., K. Chen).ORCID 0000-0003-1009-4357
Hong ChenVascular Biology Program, Boston Children's Hospital and Harvard Medical School, MA (K. Cui, B.Z., B.W., S.E.-B., A.V., H.C.).ORCID 0000-0002-1906-6611

Funding

Molecular Regulation of AtherosclerosisR01HL146134 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, SRIVASTAVA, SANJAY · 2019 to 2022
$3.3M
The role of signaling adaptor protein epsin in atherosclerosisR01HL156362 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, SHI, JINJUN · 2021 to 2024
$3.1M
The Role of Adaptor Protein Disabled-2 in Maintaining Endothelial Cell Function in AtherosclerosisR01HL162367 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, SHI, JINJUN · 2022 to 2025
$3.0M
Molecular Mechanisms Governing Vascular Cell Function and Phenotype in Health and DiseaseR01HL158097 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, CHEN, YABING · 2021 to 2024
$3.0M
Reversal of Heart Failure: Role of Vascular RecoveryR01HL148338 · NHLBI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI CHEN, KAIFU, COOKE, JOHN P · 2020 to 2023
$2.8M
Transcription Factor 4 Maintain Endothelial identity to Oppose Heart FailureR01HL155632 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI Lili Zhang · 2022 to 2026
$2.5M
Targeting Endothelial Epsins to Ameliorate Myocardial IschemiaR01HL174928 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI Hong Chen, Kaifu Chen · 2024 to 2026
$2.4M
A novel role for EZH2 in A-to-I RNA editing in prostate cancerR01CA278832 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Qi Cao, Kaifu Chen · 2024 to 2026
$2.0M
Bioinformatics Techniques to Analyze Dynamic Changes of 3D GenomeR01GM138407 · NIGMS · BOSTON CHILDREN'S HOSPITAL · PI CHEN, KAIFU · 2022 to 2025
$1.8M
Controlling Neuropilin-2 Signaling to Improve Lymphatic FunctionR01HL179216 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI DIANE Renee BIELENBERG, Hong Chen · 2025 to 2026
$1.7M
Role of S-nitrosylation in TransdifferentiationR01HL133254 · NHLBI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI CHEN, KAIFU, COOKE, JOHN P · 2018 to 2021
$1.6M
Targeting PCBP1 to Ameliorate Pathological AngiogenesisR01HL179278 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Yao Wei Lu · 2025 to 2026
$1.5M
NCI NIH HHS R01 CA278832NHLBI NIH HHS K99 HL171947NHLBI NIH HHS R01 HL133254NHLBI NIH HHS R01 HL146134NHLBI NIH HHS R01 HL148338NHLBI NIH HHS R01 HL155632NHLBI NIH HHS R01 HL156362NHLBI NIH HHS R01 HL158097NHLBI NIH HHS R01 HL162367NHLBI NIH HHS R01 HL174928NHLBI NIH HHS R01 HL177519NHLBI NIH HHS R01 HL179216NHLBI NIH HHS R01 HL179278NIGMS NIH HHS R01 GM125632NIGMS NIH HHS R01 GM138407
6 · The paper itself

Abstract

backgroundAtherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-laden foam cells and plaques within the arterial wall. Dysfunctional vascular smooth muscle cells (VSMCs), fibroblasts, endothelial cells, and macrophages contribute to disease progression. Here, we report that macrophage-specific expression of epsins, highly conserved endocytic adaptor proteins involved in clathrin-mediated endocytosis, accelerates atherosclerosis in Western diet-fed mice.

methodsWT/Apoe

resultsLysM-DKO/Apoe

conclusionsMacrophage epsin deletion limits foam cell formation and preserves VSMC and endothelial cell phenotypes and functions. These findings reveal a potential therapeutic strategy targeting macrophage epsins to combat atherosclerosis.

Indexed as

Adaptor Proteins, Vesicular TransportAortic DiseasesAtherosclerosisFoam CellsMacrophagesAnimalsCells, CulturedDisease Models, AnimalMaleMiceMice, Inbred C57BLMice, KnockoutMice, Knockout, ApoEPhenotypePlaque, AtheroscleroticSignal TransductionAdaptor Proteins, Vesicular Transportepsinatherosclerosischolesterolfoam cellsinflammationmacrophages

Identifiers

PMID40931837
PMCPMC12669475

What Socratic holds

Textmetadata
LicenceTDM
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.