Evidence map›Paper›PMID 40204950›Full record

ArticleCell death and differentiation2025

Formyl peptide receptor 1 and its antagonist T0080 in atherosclerosis.

Yu-Jing Li, Xue Zhao, Siting Wu, Nan Yao, Xueyu Zhang, Yanyan Liu, Xiaobing Tian, Yulin Li, Bin Gao, S Claiborne Johnston and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death and differentiation, 2025. 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. 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

12 authors.

Yu-Jing LiDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Xue ZhaoDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Siting WuDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Nan YaoDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Xueyu ZhangDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Yanyan LiuDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Xiaobing TianDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Yulin LiDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Bin GaoDepartment of Neurology, China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
S Claiborne JohnstonDepartment of Neurology, University of California, San Francisco, CA, 94143, USA.
Fu-Dong ShiDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China. fshi@tmu.edu.cn.ORCID 0000-0002-9675-4637
Zhiguo LiDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China. zhiguoli@tmu.edu.cn.ORCID 0000-0002-6869-2766

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82320108007National Natural Science Foundation of China (National Science Foundation of China) 82471312Tianjin Science and Technology Committee (Tianjin Municipal Science and Technology Commission) 21JCYBJC00770
6 · The paper itself

Abstract

Focal inflammation and arterial damage driven by macrophages are key pathogenic processes in atherosclerosis. However, the mechanisms that regulate these processes remain poorly understood. In this study, we demonstrate that formyl peptide receptor 1 (FPR1) agonist, a mitochondrial N-formyl peptide, is elevated in the blood of patients with atherosclerosis and correlates with carotid stenosis. Macrophages expressing FPR1 were found in atherosclerotic lesions. Conditional deletion of Fpr1 in macrophages reduced plaque formation, local inflammation, and aortic atherosclerosis in apolipoprotein E (ApoE)

Indexed as

AtherosclerosisReceptors, Formyl PeptideAnimalsApolipoproteins EHumansMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutPlaque, AtheroscleroticReactive Oxygen SpeciesApolipoproteins EFPR1 protein, humanFpr1 protein, mouseReactive Oxygen SpeciesReceptors, Formyl Peptide

Identifiers

PMID40204950
PMCPMC12501382

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.