Evidence map›Paper›PMID 40047073›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2025

FFAR4 Deficiency Increases Necrotic Cores in Advanced Lesions of ApoE

Gage M Stuttgen, Jordan M Bobek, Renee Penoske, Caris Wadding-Lee, Michael Lam, Shelby N Hader, A Phillip Owens, Daisy Sahoo

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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  2. Podocyte FFAR4 deficiency aggravated glomerular diseases and aging.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
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

8 authors.

Gage M StuttgenDepartment of Biochemistry (G.M.S., J.M.B., M.L., S.N.H., D.S.), Medical College of Wisconsin, Milwaukee.ORCID 0000-0001-5865-6000
Jordan M BobekDepartment of Biochemistry (G.M.S., J.M.B., M.L., S.N.H., D.S.), Medical College of Wisconsin, Milwaukee.
Renee PenoskeCardiovascular Center (G.M.S., J.M.B., R.P., D.S.), Medical College of Wisconsin, Milwaukee.
Caris Wadding-LeeDepartment of Internal Medicine, Division of Cardiovascular Health and Disease, University of Cincinnati, OH (C.W.-L., A.P.O.).ORCID 0000-0002-8194-8543
Michael LamDepartment of Biochemistry (G.M.S., J.M.B., M.L., S.N.H., D.S.), Medical College of Wisconsin, Milwaukee.
Shelby N HaderDepartment of Biochemistry (G.M.S., J.M.B., M.L., S.N.H., D.S.), Medical College of Wisconsin, Milwaukee.ORCID 0000-0002-6564-091X
A Phillip OwensDepartment of Internal Medicine, Division of Cardiovascular Health and Disease, University of Cincinnati, OH (C.W.-L., A.P.O.).ORCID 0000-0002-0835-620X
Daisy SahooDepartment of Biochemistry (G.M.S., J.M.B., M.L., S.N.H., D.S.), Medical College of Wisconsin, Milwaukee.ORCID 0000-0001-5210-6497

Funding

Selective Uptake and Hydrolysis of Cholesteryl Ester by SR-BIR01HL058012 · NHLBI · STATE UNIVERSITY NEW YORK STONY BROOK · PI SAHOO, DAISY · 1997 to 2023
$8.6M
The role of protease-activated receptor 2 (PAR2) in the pathogenesis of Alzheimer’s Disease (AD)R01HL141404 · NHLBI · UNIVERSITY OF CINCINNATI · PI OWENS III, ALBERT PHILLIP · 2018 to 2022
$2.4M
Unraveling the Role of Modified HDL in AtherogenesisF31HL178112 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI Jordan M Bobek · 2025 to 2026
$100k
Investigating the Novel Roles of FFAR4 in Foam Cell Formation and AtherosclerosisF31HL165927 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI STUTTGEN, GAGE M · 2023 to 2024
$93k
The role of PAR2 and HuR in programming atherosclerotic vascular smooth muscle cellsF31HL170534 · NHLBI · UNIVERSITY OF CINCINNATI · PI WADDING-LEE, CARIS ALYSSA · 2023 to 2024
$47k
American Heart Association-American Stroke Association 23PRE1019604NHLBI NIH HHS F31 HL165927NHLBI NIH HHS F31 HL170534NHLBI NIH HHS F31 HL178112NHLBI NIH HHS R01 HL058012NHLBI NIH HHS R01 HL141404
6 · The paper itself

Abstract

backgroundFFAR4 (free fatty acid receptor 4) has emerged as a target for preventing cardiovascular disease through its ability to control macrophage inflammation and foam cell formation. Previous studies have shown that FFAR4 activation can protect against the accumulation of arterial plaque buildup in atherosclerotic animal models. The goal of our study is to test the hypothesis that FFAR4 deficiency will increase atherosclerotic plaque development in

methodsMale and female

resultsFollowing 8 weeks of Western diet feeding, lesions from

conclusionsThese data suggest a novel role for FFAR4 in reducing necrotic core lesion formation and support a protective role for FFAR4 in stabilizing atherosclerotic plaques.

Indexed as

Aorta, ThoracicAortic DiseasesApolipoproteins EAtherosclerosisPlaque, AtheroscleroticReceptors, G-Protein-CoupledAnimalsDiet, WesternDisease Models, AnimalFemaleMaleMiceMice, Inbred C57BLMice, KnockoutMice, Knockout, ApoENecrosisApolipoproteins EFFAR4 protein, mouseReceptors, G-Protein-Coupledatherosclerosiscardiovascular diseasesfoam cellsinflammationmacrophages

Identifiers

PMID40047073
PMCPMC12018153

What OpenQuestion holds

Textmetadata
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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 OpenQuestion graph.