ArticleCirculation research2019
Myeloid-Specific Deletion of Epsins 1 and 2 Reduces Atherosclerosis by Preventing LRP-1 Downregulation.
Article in Circulation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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.
The trial behind it
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Who cites it
36 citing papers in PubMed, 65 citations in OpenAlex.
- GFPT2 promotes macrophage dysfunction in atherosclerosis via ACADL glycosylation-dependent suppression of ACADL and Arg1.Cellular and molecular life sciences : CMLS · 2026Article
- Endocytic Adaptor Proteins in Vascular Diseases: Critical Role of Intracellular Trafficking in Regulating Pathobiology of Vascular Disorders.Cardiology discovery · 2026Review
- Single-Cell Analysis Reveals a Critical Role for Macrophage Epsins in Regulating the Origin of Foam Cells in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Targeting Liver Epsins Ameliorates Dyslipidemia in Atherosclerosis through Inhibition of Proprotein Convertase Subtilisin/Kexin Type 9-Mediated Low-density Lipoprotein Receptor Degradation.bioRxiv : the preprint server for biology · 2025Article
- The Role of Ubiquitination on Macrophages in Cardiovascular Diseases and Targeted Treatment.International journal of molecular sciences · 2025Review
- E3 ubiquitin ligase RNF128 promotes Lys63-linked polyubiquitination on SRB1 in macrophages and aggravates atherosclerosis.Nature communications · 2025Article
- Article
- USP7 Inhibition Promotes Early Osseointegration in Senile Osteoporotic Mice.Journal of dental research · 2025Article
- Lipid droplets sequester palmitic acid to disrupt endothelial ciliation and exacerbate atherosclerosis in male mice.Nature communications · 2024Article
- Epsins oversee smooth muscle cell reprograming by influencing master regulators KLF4 and OCT4.bioRxiv : the preprint server for biology · 2024Article
- Mechanism of efferocytosis in atherosclerosis.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Elucidating the crosstalk between endothelial-to-mesenchymal transition (EndoMT) and endothelial autophagy in the pathogenesis of atherosclerosis.Vascular pharmacology · 2024Review
- Inflammation Resolution in the Cardiovascular System: Arterial Hypertension, Atherosclerosis, and Ischemic Heart Disease.Antioxidants & redox signaling · 2024Review
- Biomechanics-mediated endocytosis in atherosclerosis.Frontiers in cardiovascular medicine · 2024Review
- An update on ox-LDL-inducing vascular smooth muscle cell-derived foam cells in atherosclerosis.Frontiers in cell and developmental biology · 2024Review
- Efferocytosis in dendritic cells: an overlooked immunoregulatory process.Frontiers in immunology · 2024Review
- Article
- Cellular mechanisms underlying the impairment of macrophage efferocytosis.Immunology letters · 2023Review
- Epsin Nanotherapy Regulates Cholesterol Transport to Fortify Atheroma Regression.Circulation research · 2023Article
- Targeting Macrophage Epsins to Reverse Atherosclerosis.Circulation research · 2023Article
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 2 countries.
Funding
Abstract
rationaleAtherosclerosis is, in part, caused by immune and inflammatory cell infiltration into the vascular wall, leading to enhanced inflammation and lipid accumulation in the aortic endothelium. Understanding the molecular mechanisms underlying this disease is critical for the development of new therapies. Our recent studies demonstrate that epsins, a family of ubiquitin-binding endocytic adaptors, are critical regulators of atherogenicity. Given the fundamental contribution lesion macrophages make to fuel atherosclerosis, whether and how myeloid-specific epsins promote atherogenesis is an open and significant question.
objectiveWe will determine the role of myeloid-specific epsins in regulating lesion macrophage function during atherosclerosis. METHODS AND
resultsWe engineered myeloid cell-specific epsins double knockout mice (LysM-DKO) on an ApoE
conclusionsMyeloid epsins promote atherogenesis by facilitating proinflammatory macrophage recruitment and inhibiting efferocytosis in part by downregulating LRP-1, implicating that targeting epsins in macrophages may serve as a novel therapeutic strategy to treat atherosclerosis.
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What OpenQuestion holds
Registered trials
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.