ArticleMolecular biology reports2023
HIF-1α-PPARγ-mTORC1 signaling pathway-mediated autophagy induces inflammatory response in pancreatic cells in rats with hyperlipidemic acute pancreatitis.
Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Autophagy dysfunction in pancreatic acinar cells in acute pancreatitis: from molecular mechinery and trypsinogen activation to heterogeneity and therapeutic implications.Journal of molecular histology · 2026Review
- Research advances in hypertriglyceridemia-induced acute pancreatitis.Frontiers in medicine · 2026Review
- Tangled contacts: mitochondrial interactions with cellular organelles in acute pancreatitis.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
- Signaling Pathways Involved in Acute Pancreatitis.Journal of inflammation research · 2025Review
- Targeting the programmed cell death signaling mechanism with natural products for the treatment of acute pancreatitis: a review.Frontiers in pharmacology · 2025Review
- An in-Depth Exploration of the Genetic Interaction Network Between Ferroptosis and Acute Pancreatitis.Journal of inflammation research · 2023Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveThe incidence of hyperlipidemic acute pancreatitis (HLAP) has rapidly increased in recent years in China. Autophagy has been implicated in the inflammatory response of pancreatic cells in HLAP, but the molecular mechanisms remain unclear.
methodsIn this study, the role of HIF-1α-PPARγ-mTORC1 pathway-mediated autophagy in the inflammatory response of pancreatic cells and the underlying molecular mechanism were investigated in a rat model of HLAP using immunohistochemistry, ELISA, electron microscopy, and western blot analysis.
resultsThe results revealed that autophagy was significantly increased and pancreatic injury was exacerbated in HLAP rats, and the inflammatory response was further exacerbated by treatment with rapamycin but relieved by treatment with 3-MA. Hyperlipidemia induced upregulation of HIF-1α and downregulation of PPARγ, which in turn led to an increase in autophagy and consequently exacerbation of the inflammatory response of pancreatic cells.
conclusionsHIF-1α-PPARγ-mTORC1 pathway-mediated autophagy plays a critical role in the inflammatory response of pancreatic cells in HLAP, and interference with the HIF-1α-PPARγ-mTOR pathway can serve as a new strategy for the prevention and treatment of HLAP.
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Registered trials
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