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The incidence rate of acute pancreatitis is increasing, and severe acute pancreatitis (SAP) is associated with a high mortality rate, which may be reduced by a deeper understanding of its pathogenesis. In addition, an early determination of the severity of acute pancreatitis remains challenging. The aim of this study was to match potential biomarkers for early identification and monitoring of acute pancreatitis and to shed light on the underlying pathogenic mechanisms of SAP. The expression levels of plasma exosomal microRNA (miRNA) in patients with pancreatitis have been associated with the disease. Thus, this study compared the expression levels of exosomal miRNA in plasma collected from four patients with SAP and from four healthy participants. Analyses of the miRNA expression profiles indicated that three previously unreported miRNAs were differentially expressed in the patient group: Novel1, which was downregulated, and Novel2 and Novel3, which were upregulated. The miRNA target genes for those novel miRNAs were predicted using Metascape. Of these miRNA target genes, those that were also differentially expressed at different time points after disease induction in a mouse model of acute pancreatitis were determined. The gene for complement component 3 (C3), a target gene of Novel3, was the only gene matched in both the patient group and the mouse model. C3 appeared at most of the time points assessed after induction of acute pancreatitis in mice. These findings are foundational evidence that C3 warrants further study as an early biomarker of SAP, for investigating underlying pathogenic mechanisms of SAP, and as a therapeutic target for ameliorating the occurrence or development of SAP.
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http://dx.doi.org/10.3389/fphar.2022.980930 | DOI Listing |
Clin Exp Immunol
September 2025
Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511, Japan.
Introduction: Conventional dendritic cells (cDCs) in the gut express the vitamin A (VA)-converting enzyme retinal dehydrogenase 2 (RALDH2) and produce significant amounts of retinoic acid (RA). RA derived from gut cDCs contributes to the generation of tolerogenic responses by promoting Treg differentiation while inhibiting Th1 and Th17 cell differentiation. In this study, we investigated whether similar RA-mediated immunoregulatory mechanisms operate in the pancreas using an experimental autoimmune pancreatitis (AIP) model.
View Article and Find Full Text PDFExp Cell Res
September 2025
Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, 300100, China; Institute of Integrative Medicine for Acute Abdominal Diseases, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin 300100,
The characteristic pathological change in chronic pancreatitis (CP) is pancreatic fibrosis. In the early stages of CP development, injured acinar cells induce the infiltration of inflammatory cells, followed by pancreatic stellate cell (PSC) activation. Activated PSC induce the deposition of extracellular matrix (ECM) and promote the development of pancreatic fibrosis.
View Article and Find Full Text PDFInt J Biol Macromol
September 2025
Key Laboratory of Hepatosplenic Surgery, Ministry of Education, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Pancreatology
August 2025
Department of Dermatology, The People's Hospital of Rongchang District, Chongqing, China. Electronic address:
Gastrointest Endosc
September 2025
Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. Electronic address: