ArticleJournal of translational medicine2022
Asprosin inhibits macrophage lipid accumulation and reduces atherosclerotic burden by up-regulating ABCA1 and ABCG1 expression via the p38/Elk-1 pathway.
Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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Who cites it
34 citing papers in PubMed, 59 citations in OpenAlex.
- Daidzein Mitigates Nicotine-Induced Atherogenesis via Nrf2/ROS/TXNIP-Dependent Inhibition of Macrophage Pyroptosis and Lipid Accumulation.Molecular nutrition & food research · 2026Article
- CRISPR screening identifies DTX4 governing alveolar macrophage cholesterol efflux in pulmonary alveolar proteinosis.JCI insight · 2026Article
- Aortic asprosin overexpression does not ameliorate disease pathophysiology in a murine model of Marfan syndrome.Scientific reports · 2026Article
- TNF-α-Induced Upregulation of ADAMTS-8 Expression in SW480 Cells: Implications for Intracellular Signaling Pathways and Transcription Factor Activity.Cell biochemistry and biophysics · 2026Article
- Excitatory amino acid transporters support mast cell degranulation via α-KG-mediated methylation of Spp1.Cellular & molecular immunology · 2026Article
- Targeting IL-17 Presents a Promising Strategy for Treating Diseases Related to the Dysregulation of Lipid Homeostasis.Mediators of inflammation · 2026Review
- Three-Dimensional Perspectives on Inflammatory Regulation in Coronary Atherosclerosis: Integrated Mechanisms of Endothelial Priming, Lipid Metabolism, and Cytokine Synergy.Reviews in cardiovascular medicine · 2026Review
- Protein acetylation in atherosclerosis: beyond inflammation to core cellular processes and therapeutic potential.Frontiers in immunology · 2026Review
- Transglutaminase-2 Promotes Microglial Synaptic Phagocytosis and Ameliorates Epileptic Seizures by Inhibiting ABCA1 Ubiquitination.CNS neuroscience & therapeutics · 2025Article
- Chemerin and Asprosin as Promising Biomarkers of Metabolic Syndrome: A Scoping Review.Current obesity reports · 2025Article
- Asprosin protects against ischemia/reperfusion-induced kidney injury in mice.Journal of molecular histology · 2025Article
- Asprosin-FABP5 Interaction Modulates Mitochondrial Fatty Acid Oxidation through PPARα Contributing to MASLD Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Tissue macrophages: origin, heterogenity, biological functions, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025Review
- Targeting NINJ1-Mediated Plasma Membrane Rupture in Tubular Epithelial Cell Prevents Inflammatory Response in Acute Kidney Injury.International journal of biological sciences · 2025Article
- Identification of the LCOR-PLCL1 pathway that restrains lipid accumulation and tumor progression in clear cell renal cell carcinoma.International journal of biological sciences · 2025Article
- Macrophage-based pathogenesis and theranostics of vulnerable plaques.Theranostics · 2025Review
- Single-cell and spatial analysis reveals the interaction between ITLN1Frontiers in cardiovascular medicine · 2025Article
- Cyanidin-3-glucoside: targeting atherosclerosis through gut microbiota and anti-inflammation.Frontiers in nutrition · 2025Review
- The correlation between serum asprosin and type 2 diabetic patients with obesity in the community.Frontiers in endocrinology · 2025Article
- Indole-3-Carboxaldehyde Inhibits Inflammatory Response and Lipid Accumulation in Macrophages Through the miR-1271-5p/HDAC9 Pathway.Journal of cellular and molecular medicine · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAsprosin, a newly discovered adipokine, is a C-terminal cleavage product of profibrillin. Asprosin has been reported to participate in lipid metabolism and cardiovascular disease, but its role in atherogenesis remains elusive.
methodsAsprosin was overexpressed in THP-1 macrophage-derived foam cells and apoE
resultsExposure of THP-1 macrophages to oxidized low-density lipoprotein down-regulated asprosin expression. Lentivirus-mediated overexpression of asprosin promoted cholesterol efflux and inhibited lipid accumulation in THP-1 macrophage-derived foam cells. Mechanistic analysis revealed that asprosin overexpression activated p38 and stimulated the phosphorylation of ETS-like transcription factor (Elk-1) at Ser383, leading to Elk-1 nuclear translocation and the transcriptional activation of ATP binding cassette transporters A1 (ABCA1) and ABCG1. Injection of lentiviral vector expressing asprosin diminished atherosclerotic lesion area, increased plaque stability, improved plasma lipid profiles and facilitated RCT in apoE
conclusionAsprosin inhibits lipid accumulation in macrophages and decreases atherosclerotic burden in apoE
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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 Socratic graph.