ArticleArthritis & rheumatology (Hoboken, N.J.)2023
Lysosome-Associated Membrane Protein 3 Induces Lysosome-Dependent Cell Death by Impairing Autophagic Caspase 8 Degradation in the Salivary Glands of Individuals With Sjögren's Disease.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting lysosome-dependent cell death in cancer: towards therapeutic strategies.Biomarker research · 2026Review
- Molecular Insights into Oral Manifestations in Sjögren's Disease.International journal of molecular sciences · 2026Review
- Comprehensive analysis of programmed cell death and oridonin target identification in primary lung cancer for prognostic prediction and therapeutic strategies.Scientific reports · 2026Article
- Integrating the hallmarks of cancer into autophagy: a perspective from underlying mechanisms to therapeutic strategies.Theranostics · 2026Review
- Glycolysis inhibition functionally reprograms T follicular helper cells and reverses lupus.Cell reports · 2025Article
- Targeting metalloptosis in tumor therapy: from molecular mechanisms to application of metal nanoparticles.Molecular cancer · 2025Review
- Roles of glucagon-like peptide 1 receptor agonists in immune cell biology and autoimmune/autoinflammatory diseases.Cell & bioscience · 2025Review
- Comprehensive characterization of lysosome-dependent cell death reveals prognostic significance and immune landscape in colon adenocarcinoma.Scientific reports · 2025Article
- Article
- Mitochondrial-associated programmed-cell-death patterns for predicting the prognosis of non-small-cell lung cancer.Frontiers of medicine · 2025Article
- Updating on the Dual Role of Salivary Gland Epithelial Cell (SGEC) in Sjögren's Disease.Journal of inflammation research · 2025Review
- Semaglutide as a potential therapeutic adjunct for reducing flare-ups in Sjögren's syndrome: A case report.SAGE open medical case reports · 2025Article
- Identification of mitochondrial function and programmed cell death associated key biomarkers and the circRNA-miRNA-mRNA regulatory network in systemic lupus erythematosus.Frontiers in molecular biosciences · 2025Article
- Caspase-8 in inflammatory diseases: a potential therapeutic target.Cellular & molecular biology letters · 2024Review
- Prognostic and immunological implications of heterogeneous cell death patterns in prostate cancer.Cancer cell international · 2024Article
- Amplified Type I Interferon Response in Sjögren's Disease via Ectopic Toll-Like Receptor 7 Expression in Salivary Gland Epithelial Cells Induced by Lysosome-Associated Membrane Protein 3.Arthritis & rheumatology (Hoboken, N.J.) · 2024Article
- Therapeutic strategies of targeting non-apoptotic regulated cell death (RCD) with small-molecule compounds in cancer.Acta pharmaceutica Sinica. B · 2024Review
- Characterization of threeFrontiers in physiology · 2024Article
- PANoptosis in autoimmune diseases interplay between apoptosis, necrosis, and pyroptosis.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveLysosome-associated membrane protein 3 (LAMP3) overexpression is implicated in the development and progression of Sjögren's disease (SjD) by inducing lysosomal membrane permeabilization (LMP) and apoptotic cell death in salivary gland epithelium. The aim of this study was to clarify the molecular details of LAMP3-induced lysosome-dependent cell death and to test lysosomal biogenesis as a therapeutic intervention.
methodsHuman labial minor salivary gland biopsies were analyzed using immunofluorescence staining for LAMP3 expression levels and galectin-3 puncta formation, a marker of LMP. Expression level of caspase 8, an initiator of LMP, was determined by Western blotting in cell culture. Galectin-3 puncta formation and apoptosis were evaluated in cell cultures and a mouse model treated with glucagon-like peptide 1 receptor (GLP-1R) agonists, a known promoter of lysosomal biogenesis.
resultsGalectin-3 puncta formation was more frequent in the salivary glands of SjD patients compared to control glands. The proportion of galectin-3 puncta-positive cells was positively correlated with LAMP3 expression levels in the glands. LAMP3 overexpression increased caspase 8 expression, and knockdown of caspase 8 decreased galectin-3 puncta formation and apoptosis in LAMP3-overexpressing cells. Inhibition of autophagy increased caspase 8 expression, while restoration of lysosomal function using GLP-1R agonists decreased caspase 8 expression, which reduced galectin-3 puncta formation and apoptosis in both LAMP3-overexpressing cells and mice.
conclusionLAMP3 overexpression induced lysosomal dysfunction, resulting in lysosome-dependent cell death via impaired autophagic caspase 8 degradation, and restoring lysosomal function using GLP-1R agonists could prevent this. These findings suggested that LAMP3-induced lysosomal dysfunction is central to disease development and is a target for therapeutic intervention in SjD.
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