ArticleGastroenterology2015
Complement Component 5 Mediates Development of Fibrosis, via Activation of Stellate Cells, in 2 Mouse Models of Chronic Pancreatitis.
Article in Gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02869893 (Magnetic Resonance Cholangiopancreatography), which is not on this map. Cited by 47 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Magnetic Resonance Cholangiopancreatography (MRCP): A Reliable, Non Invasive Method for Staging Chronic Pancreatitis From Minimal Change Disease to the Advanced Stages in Pediatrics
Who cites it
47 citing papers in PubMed, 83 citations in OpenAlex.
- Complement C5a Promotes Epithelial-Mesenchymal Transition in Pterygium via C5aR Activation.Investigative ophthalmology & visual science · 2026Article
- A Novel Insight into Chronic Pancreatitis Pathogenesis: the USP1/ITGB5 Axis-Mediated Stellate Cell Activation.Inflammation · 2026Article
- Damaged glomeruli in proliferative pediatric lupus nephritis exhibit a C5a-C5aR1 induced fibrotic transcriptional program.bioRxiv : the preprint server for biology · 2026Article
- Targeting Cold-Inducible RNA-Binding Protein Attenuates Pancreatic Fibrosis by Suppressing Pyroptosis in Chronic Pancreatitis.Inflammation · 2026Article
- Statin therapy associated Lactobacillus intestinalis attenuates pancreatic fibrosis through remodeling intestinal homeostasis.NPJ biofilms and microbiomes · 2025Article
- Examination of duodenal and colonic microbiome changes in mouse models of acute and chronic pancreatitis.Scientific reports · 2024Article
- Mechanosensing Piezo channels in gastrointestinal disorders.The Journal of clinical investigation · 2023Review
- IRAK3-mediated suppression of pro-inflammatory MyD88/IRAK signaling affects disease severity in acute pancreatitis.Scientific reports · 2023Article
- 5-FU-miR-15a Inhibits Activation of Pancreatic Stellate Cells by Reducing YAP1 and BCL-2 Levels In Vitro.International journal of molecular sciences · 2023Article
- Complement and Fungal Dysbiosis as Prognostic Markers and Potential Targets in PDAC Treatment.Current oncology (Toronto, Ont.) · 2022Review
- Systemic Bile Acids Affect the Severity of Acute Pancreatitis in Mice Depending on Their Hydrophobicity and the Disease Pathogenesis.International journal of molecular sciences · 2022Article
- Therapeutic Intervention with Anti-Complement Component 5 Antibody Does Not Reduce NASH but Does Attenuate Atherosclerosis and MIF Concentrations in Ldlr-/-.Leiden Mice.International journal of molecular sciences · 2022Article
- Article
- In mouse chronic pancreatitis CD25Nature communications · 2022Article
- Complement activation contributes to subretinal fibrosis through the induction of epithelial-to-mesenchymal transition (EMT) in retinal pigment epithelial cells.Journal of neuroinflammation · 2022Article
- α2,6-Sialylation is Upregulated in Severe COVID-19 Implicating the Complement Cascade.medRxiv : the preprint server for health sciences · 2022Article
- Piezo1-mediated stellate cell activation causes pressure-induced pancreatic fibrosis in mice.JCI insight · 2022Article
- IL11 Activates Pancreatic Stellate Cells and Causes Pancreatic Inflammation, Fibrosis and Atrophy in a Mouse Model of Pancreatitis.International journal of molecular sciences · 2022Article
- Murine Chronic Pancreatitis Model Induced by Partial Ligation of the Pancreatic Duct Encapsulates the Profile of Macrophage in Human Chronic Pancreatitis.Frontiers in immunology · 2022Article
- Mobilization of CD11bFrontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsLittle is known about the pathogenic mechanisms of chronic pancreatitis. We investigated the roles of complement component 5 (C5) in pancreatic fibrogenesis in mice and patients.
methodsChronic pancreatitis was induced by ligation of the midpancreatic duct, followed by a single supramaximal intraperitoneal injection of cerulein, in C57Bl6 (control) and C5-deficient mice. Some mice were given injections of 2 different antagonists of the receptor for C5a over 21 days. In a separate model, mice were given injections of cerulein for 10 weeks to induce chronic pancreatitis. Direct effects of C5 were studied in cultured primary cells. We performed genotype analysis for the single-nucleotide polymorphisms rs 17611 and rs 2300929 in C5 in patients with pancreatitis and healthy individuals (controls). Blood cells from 976 subjects were analyzed by transcriptional profiling.
resultsDuring the initial phase of pancreatitis, levels of pancreatic damage were similar between C5-deficient and control mice. During later stages of pancreatitis, C5-deficient mice and mice given injections of C5a-receptor antagonists developed significantly less pancreatic fibrosis than control mice. Primary pancreatic stellate cells were activated in vitro by C5a. There were no differences in the rs 2300929 SNP between subjects with or without pancreatitis, but the minor allele rs17611 was associated with a significant increase in levels of C5 in whole blood.
conclusionsIn mice, loss of C5 or injection of a C5a-receptor antagonist significantly reduced the level of fibrosis of chronic pancreatitis, but this was not a consequence of milder disease in early stages of pancreatitis. C5 might be a therapeutic target for chronic pancreatitis.
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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.