ArticleAntioxidants (Basel, Switzerland)2022
Generation of Hydrogen Peroxide and Downstream Protein Kinase D1 Signaling Is a Common Feature of Inducers of Pancreatic Acinar-to-Ductal Metaplasia.
Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- ALDH1L2 regulates reactive oxygen species and acinar-to-ductal metaplasia in the pancreas.Nature metabolism · 2026Article
- NADPH-producing enzymes restrict the formation of pancreatic precancerous lesions.Nature metabolism · 2026Article
- Mitochondrial superoxide dismutase controls metabolic plasticity in pancreatic cancer.Cell communication and signaling : CCS · 2025Article
- Downregulation of Sod2 increases atypical flat lesions and dysplasia to advance pancreatic ductal adenocarcinoma.Molecular cancer · 2025Article
- Cytokine CCL9 Mediates Oncogenic KRAS-Induced Pancreatic Acinar-to-Ductal Metaplasia by Promoting Reactive Oxygen Species and Metalloproteinases.International journal of molecular sciences · 2024Article
- Protein kinase D1 - A targetable mediator of pancreatic cancer development.Biochimica et biophysica acta. Molecular cell research · 2024Review
- Macrophage-induced reactive oxygen species in the initiation of pancreatic cancer: a mini-review.Frontiers in immunology · 2024Review
- Ion channels in acinar cells in acute pancreatitis: crosstalk of calcium, iron, and copper signals.Frontiers in immunology · 2024Review
- Pancreatic acinar cell fate relies on system xCell death & disease · 2023Article
- Article
- Protein kinase D1 overexpression potentiates epidermal growth factor signaling pathway in MCF-7 cells.Molecular biology reports · 2023Article
- Roles of differently polarized macrophages in the initiation and progressionof pancreatic cancer.Frontiers in immunology · 2023Review
- Oxidative Stress in Chronic and Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Pancreatic acinar-to-ductal metaplasia (ADM) is a reversible process that occurs after pancreatic injury, but becomes permanent and leads to pancreatic lesions in the presence of an oncogenic mutation in KRAS,. While inflammatory macrophage-secreted chemokines, growth factors that activate epidermal growth factor receptor (EGFR) and oncogenic KRAS have been implicated in the induction of ADM, it is currently unclear whether a common underlying signaling mechanism exists that drives this process. In this study, we show that different inducers of ADM increase levels of hydrogen peroxide, most likely generated at the mitochondria, and upregulate the expression of Protein Kinase D1 (PKD1), a kinase that can be activated by hydrogen peroxide. PKD1 expression in acinar cells affects their survival and mediates ADM, which is in part due to the PKD1 target NF-κB. Overall, our data implicate ROS-PKD1 signaling as a common feature of different inducers of pancreatic ADM.
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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 Socratic graph.