Evidence map›Paper›PMID 34725437›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2022

FABP4 activates the JAK2/STAT2 pathway via Rap1a in the homocysteine-induced macrophage inflammatory response in ApoE

Lingbo Xu, Huiping Zhang, Yanhua Wang, Anning Yang, Xiaoyan Dong, Lingyu Gu, Dayue Liu, Ning Ding, Yideng Jiang

Open access · hybridAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% of its field
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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Lingbo Xu *Department of Pathophysiology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, China.
Huiping Zhang *National Health Commission Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan, 750004, China.
Yanhua WangNational Health Commission Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan, 750004, China.
Anning YangDepartment of Pathophysiology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, China.
Xiaoyan DongDepartment of Pathophysiology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, China.
Lingyu GuNational Health Commission Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan, 750004, China.
Dayue LiuDepartment of Pathophysiology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, China.
Ning DingNational Health Commission Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan, 750004, China.
Yideng JiangDepartment of Pathophysiology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, China. jydeng@nxmu.edu.cn.
Ningxia Medical University · CNNingxia Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a chronic inflammatory vascular disease, and inflammation plays a critical role in its formation and progression. Elevated serum homocysteine (Hcy) is an independent risk factor for atherosclerosis. Previous studies have shown that fatty acid binding protein 4 (FABP4) plays an important role in macrophage inflammation and lipid metabolism in atherosclerosis induced by Hcy. However, the underlying molecular mechanism of FABP4 in Hcy-induced macrophage inflammation remains unknown. In this study, we found that FABP4 activated the Janus kinase 2/signal transducer and activator of transcription 2 (JAK2/STAT2) pathway in macrophage inflammation induced by Hcy. Of note, we further observed that ras-related protein Rap-1a (Rap1a) induced the Tyr416 phosphorylation and membrane translocation of non-receptor tyrosine kinase (c-Src) to activate the JAK2/STAT2 pathway. In addition, the suppressor of cytokine signaling 1 (SOCS1)-a transcriptional target of signal transducer and activator of transcription (STATs) inhibited the JAK2/STAT2 pathway and Rap1a expression via a negative feedback loop. In summary, these results demonstrated that FABP4 promotes c-Src phosphorylation and membrane translocation via Rap1a to activate the JAK2/STAT2 pathway, contributing to Hcy-accelerated macrophage inflammation in ApoE

Indexed as

AnimalsApolipoproteins EAtherosclerosisCytokinesDisease Models, AnimalFatty Acid-Binding ProteinsGene Expression ProfilingHomocysteineHumansInflammation MediatorsJanus Kinase 2MacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutApolipoproteins ECytokinesFabp4 protein, mouseFatty Acid-Binding ProteinsHomocysteineInflammation MediatorsJak2 protein, mouseJanus Kinase 2Proteinsrap1 GTP-Binding ProteinsSTAT2 Transcription Factor

Identifiers

PMID34725437
PMCPMC8695379
OpenAlexW3208355829

What OpenQuestion holds

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LicenceCC BY
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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.