ArticleNature communications2024
TM4SF19-mediated control of lysosomal activity in macrophages contributes to obesity-induced inflammation and metabolic dysfunction.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 23 citations in OpenAlex.
- Unpacking adiposity: a narrative critical appraisal of diverse obesity definitions.Diabetology & metabolic syndrome · 2026Review
- Immunometabolic Dysregulation in Obesity: Integrating Macrophage Polarization, Metabolic Reprogramming, and Gut Microbiota Crosstalk.Immunity, inflammation and disease · 2026Review
- Toll-like receptor 4 signaling links cytoskeletal remodeling to lipid accumulation in macrophages.Inflammation and regeneration · 2026Review
- Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application.MedComm · 2026Review
- Driver or passenger? A new assessment of genes in the schizophrenia-associated 3q29 deletion locus for contribution to neurodevelopmental disorders.Journal of neurodevelopmental disorders · 2026Review
- Restoring Lysosomes in Adipose Tissue Macrophages Mitigates Obesity-Induced Inflammation and Insulin Resistance.International journal of molecular sciences · 2026Article
- Adipose-Tissue Macrophage Diversity and Functions.International journal of molecular sciences · 2026Review
- Obesity-induced pyroptotic adipocyte death leads to TREM2-dependent macrophage dysfunction and adipose tissue inflammation.iScience · 2026Article
- Inflammation and Resolution in Obesity-Related Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Phosphatidylethanolamine Alleviates Osteoarthritis Progression by Inhibiting Oxidative Stress-Induced Chondrocyte Ferroptosis in a Lysosomal-Dependent Manner.International journal of general medicine · 2026Article
- Lipid-Associated Macrophages in Obesity: Immunometabolic Programs and Emerging Therapeutic Implications-A Narrative Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Sequential exposure to histological chorioamnionitis and postnatal hyperoxia alters gene expression in cord blood monocytes.Frontiers in pediatrics · 2026Article
- Immunometabolism in obesity: Understanding the beneficial and detrimental roles of inflammation.PLoS biology · 2026Article
- Gut microbiota: a potential therapeutic target for hyperuricemia and gout.Bioscience of microbiota, food and health · 2026Review
- Influence of Weight Loss and Weight Regain on Adipose Tissue Inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Immunometabolic Crosstalk in Adipose Tissue Remodeling: Mechanisms and Therapeutic Perspectives.Journal of obesity & metabolic syndrome · 2025Review
- BNIP3-mediated mitophagy in macrophages regulates obesity-induced adipose tissue metaflammation.Autophagy · 2025Article
- RNA Sequencing Reveals Inflammatory and Metabolic Changes in the Lung and Brain After Carbon Black and Naphthalene Whole Body Inhalation Exposure in a Rodent Model of Military Burn Pit Exposures.International journal of molecular sciences · 2025Article
- scICE: enhancing clustering reliability and efficiency of scRNA-seq data with multi-cluster label consistency evaluation.Nature communications · 2025Article
- Radiation Promotes Acute and Chronic Damage to Adipose Tissue.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
Abstract
Adipose tissue (AT) adapts to overnutrition in a complex process, wherein specialized immune cells remove and replace dysfunctional and stressed adipocytes with new fat cells. Among immune cells recruited to AT, lipid-associated macrophages (LAMs) have emerged as key players in obesity and in diseases involving lipid stress and inflammation. Here, we show that LAMs selectively express transmembrane 4 L six family member 19 (TM4SF19), a lysosomal protein that represses acidification through its interaction with Vacuolar-ATPase. Inactivation of TM4SF19 elevates lysosomal acidification and accelerates the clearance of dying/dead adipocytes in vitro and in vivo. TM4SF19 deletion reduces the LAM accumulation and increases the proportion of restorative macrophages in AT of male mice fed a high-fat diet. Importantly, male mice lacking TM4SF19 adapt to high-fat feeding through adipocyte hyperplasia, rather than hypertrophy. This adaptation significantly improves local and systemic insulin sensitivity, and energy expenditure, offering a potential avenue to combat obesity-related metabolic dysfunction.
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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.