ArticleCirculation2015
Hck/Fgr Kinase Deficiency Reduces Plaque Growth and Stability by Blunting Monocyte Recruitment and Intraplaque Motility.
Article in Circulation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
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- High expression of Fgr in the left ventricle attenuates myocardial injury in the infarcted region via regulating the phosphorylation level of PI3K/Akt.Bioscience reports · 2025Article
- Bioinformatics Approach to Investigating the Immuno-Inflammatory Mechanisms of Periodontitis in the Progression of Atherosclerosis.Current issues in molecular biology · 2025Article
- Identification of critical endoplasmic reticulum stress-related genes in advanced atherosclerotic plaque.Scientific reports · 2025Article
- Novel biomarkers identified by weighted gene co-expression network analysis for atherosclerosis.Herz · 2024Article
- Detection of common pathogenesis of rheumatoid arthritis and atherosclerosis via microarray data analysis.Heliyon · 2024Article
- Immune-associated biomarkers identification for diagnosing carotid plaque progression with uremia through systematical bioinformatics and machine learning analysis.European journal of medical research · 2023Article
- Identification of hub genes and regulatory networks in histologically unstable carotid atherosclerotic plaque by bioinformatics analysis.BMC medical genomics · 2022Article
- Construction of genetic classification model for coronary atherosclerosis heart disease using three machine learning methods.BMC cardiovascular disorders · 2022Article
- Bioinformatics analysis of potential pathogenesis and risk genes of immunoinflammation-promoted renal injury in severe COVID-19.Frontiers in immunology · 2022Article
- Macrophages-Related Genes Biomarkers in the Deterioration of Atherosclerosis.Frontiers in cardiovascular medicine · 2022Article
- Gene deficiency or pharmacological inhibition of PDCD4-mediated FGR signaling protects against acute kidney injury.Acta pharmaceutica Sinica. B · 2021Article
- Comprehensive Analysis to Identify Key Genes Involved in Advanced Atherosclerosis.Disease markers · 2021Article
- Targeting non-coding RNAs in unstable atherosclerotic plaques: Mechanism, regulation, possibilities, and limitations.International journal of biological sciences · 2021Review
- Vascular Cells Proteome Associated with Bradykinin and Leptin Inflammation and Oxidative Stress Signals.Antioxidants (Basel, Switzerland) · 2020Article
- Value of S100A12 in predicting in-stent restenosis in patients with coronary drug-eluting stent implantation.Experimental and therapeutic medicine · 2020Article
- Identifying RBM47, HCK, CD53, TYROBP, and HAVCR2 as Hub Genes in Advanced Atherosclerotic Plaques by Network-Based Analysis and Validation.Frontiers in genetics · 2020Article
- A Promising Candidate: Heparin-Binding Protein Steps onto the Stage of Sepsis Prediction.Journal of immunology research · 2019Review
- A Novel Marker of Inflammation: Azurocidin in Patients with ST Segment Elevation Myocardial Infarction.International journal of molecular sciences · 2018Article
- Immune cell subset differentiation and tissue inflammation.Journal of hematology & oncology · 2018Review
Corrections and comments
- Erratum issued
Authors and funding
20 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundLeukocyte migration is critical for the infiltration of monocytes and accumulation of monocyte-derived macrophages in inflammation. Considering that Hck and Fgr are instrumental in this process, their impact on atherosclerosis and on lesion inflammation and stability was evaluated. METHODS AND
resultsHematopoietic Hck/Fgr-deficient, LDLr(-/-) chimeras, obtained by bone marrow transplantation, had smaller but, paradoxically, less stable lesions with reduced macrophage content, overt cap thinning, and necrotic core expansion as the most prominent features. Despite a Ly6C(high)-skewed proinflammatory monocyte phenotype, Hck/Fgr deficiency led to disrupted adhesion of myeloid cells to and transmigration across endothelial monolayers in vitro and atherosclerotic plaques in vivo, as assessed by intravital microscopy, flow cytometry, and histological examination of atherosclerotic arteries. Moreover, Hck/Fgr-deficient macrophages showed blunted podosome formation and mesenchymal migration capacity. In consequence, transmigrated double-knockout macrophages were seen to accumulate in the fibrous cap, potentially promoting its focal erosion, as observed for double-knockout chimeras.
conclusionsThe hematopoietic deficiency of Hck and Fgr led to attenuated atherosclerotic plaque formation by abrogating endothelial adhesion and transmigration; paradoxically, it also promoted plaque instability by causing monocyte subset imbalance and subendothelial accumulation, raising a note of caution regarding src kinase-targeted intervention in plaque inflammation.
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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.