ArticleCellular and molecular gastroenterology and hepatology2015
Lysosome associated membrane proteins maintain pancreatic acinar cell homeostasis: LAMP-2 deficient mice develop pancreatitis.
Article in Cellular and molecular gastroenterology and hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.
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93 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.
- MiRNA-loaded MSC exosomes restore autophagy flux for acute pancreatitis therapy.Frontiers in immunology · 2025Pooled it
- Genetic and pharmacologic modulations elucidate NRF2 protective role in acute pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Loss of the ER-cargo protein CLN8 increases severity of acute pancreatitis and upregulates ER-stress and ER-phagy.Molecular biomedicine · 2026Article
- Association between the geriatric nutritional risk index and all-cause mortality in patients with acute pancreatitis in the intensive care unit: a retrospective cohort study.Scientific reports · 2026Article
- Cell death and its interaction with mitochondrial dysfunction in pathogenesis of acute pancreatitis: a comprehensive review.Apoptosis : an international journal on programmed cell death · 2026Review
- From single-pathway cascade to network pathophysiology: how genetically engineered mouse models reshaped our understanding of pancreatitis.Frontiers in physiology · 2026Review
- The Role of Macrophages in Acute Pancreatitis: From Inflammatory Drivers to Therapeutic Targets.International journal of medical sciences · 2026Review
- A review of autophagy in the pancreas: normal physiology and pathophysiology.Autophagy reports · 2026Review
- Understanding Liver and Digestive Diseases: A Paved Road to Improve Diagnosis, Management, and Treatment.Exploration of digestive diseases · 2026Article
- Reprogramming of cholesterol sensing in epithelial cells supports pancreatic inflammation.Molecular metabolism · 2026Article
- Post-translational modification crosstalk in acute pancreatitis: linking acinar stress to innate immune amplification and tissue repair.Frontiers in immunology · 2026Review
- Apoptotic extracellular vesicles from peripancreatic adipose-derived mesenchymal stem cells ameliorate severe acute pancreatitis through the transcription factor EB-mediated autophagy-lysosomal pathway: an experimental study.International journal of surgery (London, England) · 2025Article
- Pancreatic involvement inMolecular genetics and metabolism reports · 2025Article
- Rescuing lysosomal/autophagic defects via nanoapproach: implications for lysosomal/autophagic defect-related diseases.Journal of Zhejiang University. Science. B · 2025Review
- Pharmacological Inhibition of Phosphoglycerate Kinase 1 Reduces OxiDative Stress and Restores Impaired Autophagy in Experimental Acute Pancreatitis.Inflammation · 2025Article
- Dysfunction of Autophagy in Adipose Tissue Macrophages Regulated via FoxO1 in Obesity-Related Severe Acute Pancreatitis.International journal of molecular sciences · 2025Article
- Global insights and knowledge mapping of immunity and inflammation in acute pancreatitis: A bibliometric and visual analysis.Medicine · 2025Article
- The transcription factors Tfeb and Tfe3 are required for survival and embryonic development of pancreas and liver in zebrafish.PLoS genetics · 2025Article
- Targeted animal models for preclinical assessment of cellular and gene therapies in pancreatic and liver diseases: regulatory and practical insights.Cytotherapy · 2025Review
- From micro to macro, nanotechnology demystifies acute pancreatitis: a new generation of treatment options emerges.Journal of nanobiotechnology · 2025Review
33 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 6 institutions in 4 countries.
Funding
Abstract
BACKGROUND &
aimsThe pathogenic mechanism of pancreatitis is poorly understood. Recent evidence implicates defective autophagy in pancreatitis responses; however, the pathways mediating impaired autophagy in pancreas remain largely unknown. Here, we investigate the role of lysosome associated membrane proteins (LAMPs) in pancreatitis.
methodsWe analyzed changes in LAMPs in experimental models and human pancreatitis, and the underlying mechanisms: LAMP de-glycosylation and degradation. LAMP cleavage by cathepsin B (CatB) was analyzed by mass spectrometry. We used mice deficient in LAMP-2 to assess its role in pancreatitis.
resultsPancreatic levels of LAMP-1 and LAMP-2 greatly decrease across various pancreatitis models and in human disease. Pancreatitis does not trigger LAMPs' bulk de-glycosylation, but induces their degradation via CatB-mediated cleavage of LAMP molecule close to the boundary between luminal and transmembrane domains. LAMP-2 null mice spontaneously develop pancreatitis that begins with acinar cell vacuolization due to impaired autophagic flux, and progresses to severe pancreas damage characterized by trypsinogen activation, macrophage-driven inflammation, and acinar cell death. LAMP-2 deficiency causes a decrease in pancreatic digestive enzymes content, stimulates the basal and inhibits CCK-induced amylase secretion by acinar cells. The effects of LAMP-2 knockout and acute cerulein pancreatitis overlap, which corroborates the pathogenic role of LAMP decrease in experimental pancreatitis models.
conclusionsThe results indicate a critical role for LAMPs, particularly LAMP-2, in maintaining pancreatic acinar cell homeostasis, and provide evidence that defective lysosomal function, resulting in impaired autophagy, leads to pancreatitis. Mice with LAMP-2 deficiency present a novel genetic model of human pancreatitis caused by lysosomal/autophagic dysfunction.
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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.