ArticleCardiovascular research2016
Enhanced atheroprotection and lesion remodelling by targeting the foam cell and increasing plasma cholesterol acceptors.
Article in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Spatial transcriptomics maps distinct signatures of human intermuscular adipose expansion in mice.medRxiv : the preprint server for health sciences · 2026Article
- From Storage to Signaling: Lipid Droplet Lipolysis in Cholesterol Mobilization and Foam Cell Remodeling.Current atherosclerosis reports · 2026Review
- Article
- Regulation of Monocyte Perilipin-2 Expression in Acute and Chronic Coronary Syndromes: Pathogenetic Implications.International journal of molecular sciences · 2025Article
- Single-cell and spatial analysis reveals the interaction between ITLN1Frontiers in cardiovascular medicine · 2025Article
- Lipid droplet-associated hydrolase mobilizes stores of liver X receptor sterol ligands and protects against atherosclerosis.Nature communications · 2024Article
- Drug screen identifies verteporfin as a regulator of lipid metabolism in macrophage foam cells.Scientific reports · 2023Article
- Article
- Integrated Transcriptome and 16S rDNA Analyses Reveal That Transport Stress Induces Oxidative Stress and Immune and Metabolic Disorders in the Intestine of Hybrid Yellow Catfish (Antioxidants (Basel, Switzerland) · 2022Article
- Lipid Droplet-Related PLIN2 in CD68Frontiers in oncology · 2022Article
- Serum Perilipin 2 (PLIN2) Predicts Multiple Organ Dysfunction in Critically Ill Patients.Biomedicines · 2021Article
- Short-Term Acyl-CoA:Cholesterol Acyltransferase Inhibition, Combined with Apoprotein A1 Overexpression, Promotes Atherosclerosis Inflammation Resolution in Mice.Molecular pharmacology · 2021Article
- Light-Dark Patterns Mirroring Shift Work Accelerate Atherosclerosis and Promote Vulnerable Lesion Phenotypes.Journal of the American Heart Association · 2021Article
- The Expression of Perilipin Family Proteins can be used as Diagnostic Markers of Liposarcoma and to Differentiate Subtypes.Journal of Cancer · 2020Article
- Synergetic Effect of rHDL and LXR Agonist on Reduction of Atherosclerosis in Mice.Frontiers in pharmacology · 2020Article
- UVA Induced Oxidative Stress Was Inhibited by Paeoniflorin/Nrf2 Signaling or PLIN2.Frontiers in pharmacology · 2020Article
- Cholesterol Acceptors Regulate the Lipidome of Macrophage Foam Cells.International journal of molecular sciences · 2019Article
- HDL and Reverse Cholesterol Transport.Circulation research · 2019Review
- Roles of Perilipins in Diseases and Cancers.Current genomics · 2018Article
- Dysfunctional HDL in diabetes mellitus and its role in the pathogenesis of cardiovascular disease.Molecular and cellular biochemistry · 2018Review
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Abstract
aimsAtherosclerosis development can be ameliorated by promoting reverse cholesterol transport (RCT) from arteries. The process involves cholesterol efflux from foam cells to extracellular acceptors such as apolipoprotein A-I (apoA-I) and high-density lipoprotein (HDL) that mediate transport to the liver. Perilipin-2 (PLIN2) is a lipid droplet (LD)-associated protein that in macrophages facilitates cholesterol storage and prevents efflux. We hypothesized that atheroprotection would be enhanced by concurrently targeting PLIN2 to increase the efflux capacity of foam cells and increasing plasma apoA-I and HDL. METHODS AND
resultsPLIN2-knockout and wild-type mice lacking apolipoprotein E (PLIN2(-/-)/apoE(-/-) and PLIN2(+/+)/apoE(-/-)) were treated with a helper-dependent adenoviral vector encoding human apoA-I (HDAd-AI) or with control empty vector. Treatment with HDAd-AI increased hepatic apoA-I production, plasma apoA-I and HDL-cholesterol (HDL-C), and apoA-I deposition in lesions to a similar extent in PLIN2(-/-)/apoE(-/-) and PLIN2(+/+)/apoE(-/-) mice. However, atherosclerosis development at the aortic sinus was considerably lower in HDAd-AI-treated PLIN2(-/-)/apoE(-/-) mice. A more stable lesion phenotype, with increased collagen content, was primarily associated to treatment with HDAd-AI, but was enhanced under PLIN2 deficiency. PLIN2 deficiency and apoA-I cumulatively reduced LDs and cholesterol ester content in cultured macrophages. Neutral lipid in atheroma was significantly reduced in HDAd-AI-treated PLIN2(-/-)/apoE(-/-) mice, and RCT from macrophages to feces was enhanced in PLIN2(-/-) macrophages.
conclusionThese studies demonstrate a mutually beneficial relationship between PLIN2 deficiency and elevated apoA-I/HDL-C in preventing atherosclerosis development. The data support that targeting foam cell components to mobilize cholesterol may be a promising strategy to enhance the atheroprotection of plasma cholesterol acceptors.
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