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Pancreatic Diseases: Molecular Pathology and Therapeutics
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Pancreatic Diseases: Molecular Pathology and Therapeutics

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 May 2026) | Viewed by 3059

Editor

Prof. Dr. Maria Ines Vaccaro

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals

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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

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Published Papers (2 papers)

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Research

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15 pages, 3531 KB  
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
Cited by 2 | Viewed by 1626
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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Review

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22 pages, 2564 KB  
Review
From Inflammation to Neuroplasticity: Molecular Mechanisms of Pain in Acute, Recurrent and Chronic Pancreatitis
by Cristina Patoni, Stella Ioana Popescu, Christopher Pavel, Marius Nicolae Popescu and Cristian Gheorghe
Int. J. Mol. Sci. 2026, 27(14), 6383; https://doi.org/10.3390/ijms27146383 - 17 Jul 2026
Viewed by 715
Abstract
Pain is the most significant and debilitating symptom throughout all stages of pancreatitis, yet the precise mechanisms responsible for it remain only partially understood, and current pain relief methods often prove insufficient. To gain a clearer understanding, it is crucial to consider pancreatitis [...] Read more.
Pain is the most significant and debilitating symptom throughout all stages of pancreatitis, yet the precise mechanisms responsible for it remain only partially understood, and current pain relief methods often prove insufficient. To gain a clearer understanding, it is crucial to consider pancreatitis not as a singular condition but as comprising three distinct clinical types: acute pancreatitis (AP), recurrent acute pancreatitis (RAP), and chronic pancreatitis (CP), each of which may involve different pathways for pain perception. Notably, RAP has historically been overlooked as a distinct entity, resulting in a paucity of phenotype-specific data regarding its pain mechanisms. At the molecular level, pain in pancreatitis involves peripheral and central sensitization, neuroinflammatory signaling, and structural neural remodeling, processes driven by mediators such as substance P, CGRP, NGF, TRP channels, and pro-inflammatory cytokines. However, these mechanisms have been studied largely in isolation and within single phenotypes, leaving a critical gap in our understanding of how they evolve and interact across the full disease spectrum. This review aims to establish a comprehensive framework detailing the molecular mechanisms responsible for pain in all three pancreatitis phenotypes, with a particular focus on RAP as a less-studied clinical condition and to identify phenotype-specific targets for therapeutic development. Full article
(This article belongs to the Special Issue Pancreatic Diseases: Molecular Pathology and Therapeutics)
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