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Pancreatic Diseases: Molecular Pathology and Therapeutics

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Guest Editor
National Council for Scientific and Technical Research, Center for Medical Education and Clinical Research University Institute, University of Buenos Aires, Buenos Aires C1180, Argentina
Interests: autophagy; selective autophagy; secretory autophagy; physiology; pathophysiology; pancreatic diseases
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Special Issue Information

Dear Colleagues,

This Special Issue delves into the intricate molecular mechanisms underlying pancreatic diseases, highlighting advances in the understanding of these pathologies and therapeutic strategies. Unravelling the complexities of the pathophysiological mechanisms of pancreatic diseases by focusing on the search for molecular markers, genetic predispositions, and cellular interactions is pertintent to this. By bridging the gap between molecular pathology and clinical applications, this issue aims to foster new diagnostic tools and treatments that improve patient outcomes. Contributions from diverse disciplines are expected to provide a comprehensive perspective on pancreatic diseases, with an emphasis on translational research that could lead to advances in the treatment of diseases such as pancreatic cancer, diabetes, and acute and chronic pancreatitis. Original research papers and review articles are welcome.

Prof. Dr. Maria Ines Vaccaro
Guest Editor

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Keywords

  • pancreatic cancer
  • acute pancreatitis
  • chronic pancreatitis
  • diabetes
  • inflammation
  • molecular markers
  • therapeutic strategies
  • genetic predispositions
  • diagnostic tools

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Published Papers (1 paper)

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Research

15 pages, 3531 KiB  
Article
VMP1 Constitutive Expression in Mice Dampens Pancreatic and Systemic Histopathological Damage in an Experimental Model of Severe Acute Pancreatitis
by Veronica Boggio, Claudio Daniel Gonzalez, Elsa Zotta, Alejandro Ropolo and Maria Ines Vaccaro
Int. J. Mol. Sci. 2025, 26(7), 3196; https://doi.org/10.3390/ijms26073196 - 29 Mar 2025
Viewed by 243
Abstract
Acute pancreatitis (AP) an inflammatory condition caused by the premature activation of pancreatic proteases, leads to organ damage, systemic inflammation, and multi-organ failure. Severe acute pancreatitis (SAP) has high morbidity and mortality, affecting the liver, kidneys, and lungs. Autophagy maintains pancreatic homeostasis, with [...] Read more.
Acute pancreatitis (AP) an inflammatory condition caused by the premature activation of pancreatic proteases, leads to organ damage, systemic inflammation, and multi-organ failure. Severe acute pancreatitis (SAP) has high morbidity and mortality, affecting the liver, kidneys, and lungs. Autophagy maintains pancreatic homeostasis, with VMP1-mediated selective autophagy (zymophagy) preventing intracellular zymogen activation and acinar cell death. This study examines the protective role of VMP1 (Vacuole Membrane Protein 1)-induced autophagy using ElaI-VMP1 transgenic mice in a necrohemorrhagic SAP model (Hartwig’s model). ElaI-VMP1 mice show significantly reduced pancreatic injury, including lower necrosis, edema, and inflammation, compared to wild-type (WT) mice. Biochemical markers (lactate dehydrogenase-LDH-, amylase, and lipase) and histopathology confirm that VMP1 expression mitigates pancreatic damage. Increased zymophagy negatively correlates with acinar necrosis, reinforcing its protective role. Beyond the pancreas, ElaI-VMP1 mice exhibit preserved liver, kidney, and lung histology, indicating reduced systemic organ damage. The liver maintains normal architecture, kidneys show minimal tubular necrosis, and lung inflammation features are reduced compared to WT mice. Our results confirm that zymophagy functions as a protective pathophysiological mechanism against pancreatic and extrapancreatic tissue injury in SAP. Further studies on the mechanism of VMP1-mediated selective autophagy in AP are necessary to determine its relevance and possible modulation to prevent the severity of AP. Full article
(This article belongs to the Special Issue Pancreatic Diseases: Molecular Pathology and Therapeutics)
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