ArticleScience signaling2024
Designer high-density lipoprotein particles enhance endothelial barrier function and suppress inflammation.
Article in Science signaling, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
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.
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Who cites it
15 citing papers in PubMed, 14 citations in OpenAlex.
- APOM-associated inflammation and apoptosis in stroke-exacerbated myocardial infarction: implications for brain-heart interactions.Apoptosis : an international journal on programmed cell death · 2026Article
- Application of nanotherapy in cardiovascular diseases featuring novel pharmacological mechanisms and drug delivery strategies.Discover nano · 2026Review
- Modulation of the Apolipoprotein M/S1PR4 Pathway Reduces Podocyte Lipid Overload in Alport Syndrome via Distinct Autophagy and Efflux Mechanisms.Journal of the American Society of Nephrology : JASN · 2026Article
- Apolipoprotein M: Structural insights, functional roles, and therapeutic approaches in vascular disease.The Journal of biological chemistry · 2026Review
- The potential effect of albumin replacement on immune modulation and sphingosine 1-phosphate dynamics.Scientific reports · 2026Observational
- Blood-borne sphingosine 1-phosphate maintains vascular resistance, blood pressure, and cardiac function in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Focusing on the Apolipoprotein M-Mitophagy Axis: A Mechanism for Renal Protection in Diabetic Nephropathy.Journal of diabetes research · 2026Review
- Comparative associations of immune-inflammatory, immune-lipid, and metabolic composite indices with hyperuricemia among Chinese adults with glycemic abnormalities: a health examination-based cross-sectional study.Frontiers in endocrinology · 2026Observational
- ApoA1/HDL and sepsis-associated vascular endothelial injury: a narrative review.Critical care (London, England) · 2025Review
- Ceramides in cardiovascular disease: emerging role as independent risk predictors and novel therapeutic targets.Cardiovascular research · 2025Review
- ApoM-bound S1P acts via endothelial S1PR1 to suppress choroidal neovascularization and vascular leakage.Angiogenesis · 2025Article
- ApoM and Major Adverse Cardiovascular Events in Chronic Kidney Disease: A Prospective Cohort Study.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Inflammatory lipid biomarkers and transplant-free mortality risk in hepatitis B-related cirrhosis and hepatic encephalopathy.Frontiers in medicine · 2025Article
- Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives.Frontiers in pharmacology · 2025Review
- Article
Corrections and comments
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Authors and funding
21 authors at 8 institutions in 4 countries.
Funding
Abstract
High-density lipoprotein (HDL) nanoparticles promote endothelial cell (EC) function and suppress inflammation, but their utility in treating EC dysfunction has not been fully explored. Here, we describe a fusion protein named ApoA1-ApoM (A1M) consisting of apolipoprotein A1 (ApoA1), the principal structural protein of HDL that forms lipid nanoparticles, and ApoM, a chaperone for the bioactive lipid sphingosine 1-phosphate (S1P). A1M forms HDL-like particles, binds to S1P, and is signaling competent. Molecular dynamics simulations showed that the S1P-bound ApoM moiety in A1M efficiently activated EC surface receptors. Treatment of human umbilical vein ECs with A1M-S1P stimulated barrier function either alone or cooperatively with other barrier-enhancing molecules, including the stable prostacyclin analog iloprost, and suppressed cytokine-induced inflammation. A1M-S1P injection into mice during sterile inflammation suppressed neutrophil influx and inflammatory mediator secretion. Moreover, systemic A1M administration led to a sustained increase in circulating HDL-bound S1P and suppressed inflammation in a murine model of LPS-induced endotoxemia. We propose that A1M administration may enhance vascular endothelial barrier function, suppress cytokine storm, and promote resilience of the vascular endothelium.
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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 OpenQuestion graph.