ArticleJournal of advanced research2025
Deficiency of myeloid NPC1 exacerbates liver injury and fibrosis by impairing macrophage efferocytosis.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Solute Carrier Family 1 Member 5 (SLC1A5)-dependent glutamine transport regulates macrophage senescence and efferocytosis during liver regeneration.Molecular biomedicine · 2026Article
- Article
- Article
- Review
- cGAS-STING signaling pathway in MASLD and liver fibrosis.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Efferocytosis in heart failure: Mechanisms, dysregulation and therapeutic potential.Theranostics · 2026Review
- Targeting efferocytosis for tissue regeneration: From microenvironment reprogramming to clinical translation.Theranostics · 2026Review
- From inflammatory activation to fibrotic remodeling: the central role of macrophage heterogeneity in frozen shoulder.Frontiers in immunology · 2026Review
- The Niemann-Pick C1 Protein of Patients with Hepatocellular Carcinoma Is Associated with Survival Time in Males and Tumor Size in Females.Biomedicines · 2025Article
- Mechanical stress contributes to ligamentum flavum hypertrophy by inducing local inflammation and myofibroblast transition in the innovative surgical rabbit model.Frontiers in immunology · 2025Article
- The Role of Mitochondrial Quality Control in Liver Diseases: Dawn of a Therapeutic Era.International journal of biological sciences · 2025Review
- Macrophage heterogeneity in liver fibrosis.Frontiers in immunology · 2025Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionNiemann-Pick C1 (NPC1), a lysosomal cholesterol transport protein, is required for efficient efferocytosis. Patients with Npc1 mutation are frequently accompanied with hepatic symptoms, including hepatomegaly, elevated liver transaminases, or even acute liver failure, but the pathogenic mechanism remains unknown.
objectivesOur work aims to characterize the functional role of myeloid NPC1 in liver injury and elucidate its underlying mechanism.
methodsAnalyses of injured livers from patients with liver diseases and mouse models were conducted to examine NPC1 expression. Myeloid cell-specific Npc1 knockout mice were constructed to determine the functional role of macrophage NPC1 in liver injury. Isolated macrophages were subjected to in vitro mechanistical assays.
resultsWe found that NPC1 is mainly expressed in hepatic macrophages. Its mRNA and protein expression are significantly elevated in injured livers from both patients and mouse models. Tissue-specific deletion of myeloid Npc1 increased liver inflammation, levels of serum liver function enzymes, and liver fibrosis in mouse models of liver injury induced by carbon tetrachloride (CCl
conclusionsThese findings indicate that elevated expression of myeloid NPC1 in liver diseases protects liver from injury by promoting macrophage efferocytosis of damaged cells. Dysfunction of NPC1 aggravates liver injury, suggesting that NPC1 may be a potential therapeutic target for treating liver diseases.
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