ArticleCellular and molecular life sciences : CMLS2022
Perilipin-2 limits remyelination by preventing lipid droplet degradation.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 51 citations in OpenAlex.
- High follicular fluid levels of 25-hydroxycholesterol might lead to increased number of lipid droplets in granulosa cells in polyendocrine metabolic ovarian syndrome (PMOS): a hypothesis.Journal of endocrinological investigation · 2026Article
- Convergent Astrocytic Failure in Parkinson's Disease: A System-Level Model of Pathogenesis and Treatment.Molecular neurobiology · 2026Review
- METTL3 Promotes Lipid Deposition and Pulmonary Fibrosis by Destabilizing PLIN2 in a m6A-Dependent Manner.Journal of cellular and molecular medicine · 2026Article
- PLIN2-PGAM5-regulated lipid droplet-mitochondria contacts drive microglial neuroinflammation after spinal cord injury via fatty acid metabolic reprogramming.Cell death and differentiation · 2026Article
- Lactate alleviates early brain damage after subarachnoid hemorrhage: Regulation of lipid metabolism.Neural regeneration research · 2026Article
- An Aqueous Extract ofInternational journal of molecular sciences · 2026Article
- Macrophage FTO deficiency accelerates atherosclerosis via PACS2-mediated activation of the PPARγ lipid signaling pathway.Journal of translational medicine · 2026Article
- Obesity supersizes macrophage and neutrophil activation after stroke while lipid droplets play a protective role.Journal of neuroinflammation · 2026Article
- Cellular mechanisms of brain lipid metabolism in health and disease.Nature cell biology · 2026Review
- Review
- Simvastatin Ameliorates Lipid Metabolism-Mediated Endothelial Inflammation and Tight Junction Impairment in Chronic Cerebral Hypoperfusion.Neuromolecular medicine · 2026Article
- AXL Promotes Ischemic Myelin Repair Through Alleviating Myelin Debris Deposition and Lipid Droplets Accumulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Bioinformatic characterization and automated detection of metabolically activated monocyte subpopulations in dyslipidemia.Scientific reports · 2026Article
- Autophagy-NLRP3 Inflammasome Crosstalk in Microglia: A Therapeutic Target for Multiple Sclerosis.Inflammation · 2026Review
- Microglial handling of myelin debris and remyelination after ischaemic stroke: recognition, intracellular processing, lipid fate, and oligodendroglial repair.Frontiers in cellular neuroscience · 2026Review
- Navigating the Lipid Landscape: The Role of Fatty Acid Synthase in Neural Stem Cell Fate and Central Nervous System Function.Molecular neurobiology · 2025Review
- Cancer-associated fibroblast-derived extracellular vesicles regulate lipophagy through PLIN2 to modulate dormancy in salivary gland adenoid cystic carcinoma cells.Experimental & molecular medicine · 2025Article
- Article
- Role of lipid droplets in pulmonary arterial hypertension: focusing on pulmonary artery smooth muscle cell proliferation.Lipids in health and disease · 2025Review
- Accumulation of lipids after acute direct and indirect traumatic injuries in male and female mice.BMC musculoskeletal disorders · 2025Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Foamy macrophages and microglia containing lipid droplets (LDs) are a pathological hallmark of demyelinating disorders affecting the central nervous system (CNS). We and others showed that excessive accumulation of intracellular lipids drives these phagocytes towards a more inflammatory phenotype, thereby limiting CNS repair. To date, however, the mechanisms underlying LD biogenesis and breakdown in lipid-engorged phagocytes in the CNS, as well as their impact on foamy phagocyte biology and lesion progression, remain poorly understood. Here, we provide evidence that LD-associated protein perilipin-2 (PLIN2) controls LD metabolism in myelin-containing phagocytes. We show that PLIN2 protects LDs from lipolysis-mediated degradation, thereby impairing intracellular processing of myelin-derived lipids in phagocytes. Accordingly, loss of Plin2 stimulates LD turnover in foamy phagocytes, driving them towards a less inflammatory phenotype. Importantly, Plin2-deficiency markedly improves remyelination in the ex vivo brain slice model and in the in vivo cuprizone-induced demyelination model. In summary, we identify PLIN2 as a novel therapeutic target to prevent the pathogenic accumulation of LDs in foamy phagocytes and to stimulate remyelination.
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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.