ArticleFrontiers in immunology2022
Acinar Cell-Derived Extracellular Vesicle MiRNA-183-5p Aggravates Acute Pancreatitis by Promoting M1 Macrophage Polarization Through Downregulation of FoxO1.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Acute pancreatitis: mechanisms and therapeutic approaches.Signal transduction and targeted therapy · 2026Review
- The Role of Macrophages in Acute Pancreatitis: From Inflammatory Drivers to Therapeutic Targets.International journal of medical sciences · 2026Review
- Nanoscale Delivery of MicroRNAs via Extracellular Vesicles: Mechanisms Potential in Modulating Cellular Senescence.International journal of nanomedicine · 2026Review
- Uncovering new MicroRNAs linked to acute pancreatitis: zeroing in on the protective effect.Hereditas · 2025Article
- Exosomal miRNAs in pancreatitis: Mechanisms and potential applications (Review).Molecular medicine reports · 2025Review
- Ulinastatin inhibits macrophage M1 polarization to improve acute pancreatitis-associated intestinal barrier dysfunction by promoting Nrf2 signaling pathway activation.European journal of medical research · 2025Article
- Inhibition of Zbp1-PANoptosome-mediated PANoptosis effectively attenuates acute pancreatitis.Cell death discovery · 2025Article
- Identification of Grb2 protein as a potential mediator of macrophage activation in acute pancreatitis based on bioinformatics and experimental verification.Frontiers in immunology · 2025Article
- METTL14 decreases FTH1 mRNA stability via m6A methylation to promote sorafenib-induced ferroptosis of cervical cancer.Cancer biology & therapy · 2024Article
- Noncoding Ribonucleic Acids (RNAs) May Improve Response to Immunotherapy in Pancreatic Cancer.ACS pharmacology & translational science · 2024Review
- Roles of extracellular vesicles on macrophages in inflammatory bone diseases.Molecular and cellular biochemistry · 2024Review
- The Pivotal Role of Macrophages in the Pathogenesis of Pancreatic Diseases.International journal of molecular sciences · 2024Review
- Mitochondrial (mt)DNA-cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling promotes pyroptosis of macrophages via interferon regulatory factor (IRF)7/IRF3 activation to aggravate lung injury during severe acute pancreatitis.Cellular & molecular biology letters · 2024Article
- Pancreatic Crosstalk in the Disease Setting: Understanding the Impact of Exocrine Disease on Endocrine Function.Comprehensive Physiology · 2024Review
- circ_UTRN inhibits ferroptosis of ARJ21 cells to attenuate acute pancreatitis progression by regulating the miR-760-3p/FOXO1/GPX4 axis.3 Biotech · 2024Article
- Plasma Exosomes Aggravate Acute Pancreatitis by Promoting M1 Polarization of Adipose Tissue Macrophages in Obesity-Related Severe Acute Pancreatitis.Digestive diseases and sciences · 2023Article
- The Role of MicroRNAs in Pancreatitis Development and Progression.International journal of molecular sciences · 2023Review
- Emodin Ameliorates Severe Acute Pancreatitis-Associated Acute Lung Injury in Rats by Modulating Exosome-Specific miRNA Expression Profiles.International journal of nanomedicine · 2023Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute pancreatitis (AP) is a common cause of a clinically acute abdomen. Crosstalk between acinar cells and leukocytes (especially macrophages) plays an important role in the development of AP. However, the mechanism mediating the interaction between acinar cells and macrophages is still unclear. This study was performed to explore the role of acinar cell extracellular vesicles (EVs) in the crosstalk between acinar cells and macrophages involved in the pathogenesis of AP. EVs derived from caerulein-treated acinar cells induced macrophage infiltration and aggravated pancreatitis in an AP rat model. Further research showed that acinar cell-derived EV miR-183-5p led to M1 macrophage polarization by downregulating forkhead box protein O1 (FoxO1), and a dual-luciferase reporter assay confirmed that FoxO1 was directly inhibited by miR-183-5p. In addition, acinar cell-derived EV miR-183-5p reduced macrophage phagocytosis. Acinar cell-derived EV miR-183-5p promoted the pancreatic infiltration of M1 macrophages and increased local and systemic damage
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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.