ArticleProceedings of the National Academy of Sciences of the United States of America2025
Lipid raft proteomics identify endothelial myosin-9 (MYH9) as a regulator of low-density lipoprotein transcytosis and atherosclerosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. 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 4 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.
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Who cites it
4 citing papers in PubMed.
- Therapeutic Target Mapping to Advance Drug Repurposing for Cardiovascular Disease: A Perspective from an Explanted Heart Biobank.Journal of personalized medicine · 2026Review
- PER2 reprograms intracellular cholesterol synthesis to inhibit oral squamous cell carcinoma and the chronotherapeutic efficacy of simvastatin.Cell death discovery · 2026Article
- Targeting caveolin-1: dual challenges in tumor immunity and drug therapy strategies.Cancer cell international · 2026Review
- The excitatory neurotransmitter glutamate and its receptors: the culprits behind neuropathic pain?Frontiers in aging neuroscience · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors.
Funding
Abstract
backgroundIn early atherosclerosis, circulating Low-Density Lipoprotein (LDL) crosses the endothelium by transcytosis. This involves caveolar uptake of LDL by scavenger receptor BI (SR-BI) and activin-like kinase 1 (ALK1) and requires the protein caveolin-1 (Cav-1). We identified mediators of LDL transcytosis by isolating membrane microdomains enriched in caveolin-1 from human coronary endothelial cells (HCAECs) treated with LDL and performing mass spectrometry. One of the proteins identified was myosin-9 (MYH9).
methodsTotal internal reflection fluorescence microscopy was conducted to measure LDL transcytosis by HCAECs. We measured LDL transcytosis in vivo in mice lacking endothelial MYH9 (EC-
resultsGene ontology analysis in human aortic endothelial cells suggested a role for MYH9 in exocytosis. Both knockdown and pharmacologic inhibition of MYH9 inhibited LDL transcytosis. MYH9 depletion caused an accumulation of LDL-containing vesicles at the base of the cell; overexpression caused an increase in LDL exocytosis. EC-
conclusionsLipid raft proteomics identified MYH9 as a regulator of LDL transcytosis. MYH9 is required for endothelial LDL exocytosis and contributes to early atherosclerosis.
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Registered trials
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