Novel Insights into the Molecular Mechanisms in Pancreatitis

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 2071

Special Issue Editor


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Guest Editor
Division of Digestive and Liver Diseases, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA
Interests: pancreatic cellular physiology; mechanism of pancreatic diseases; acute pancreatitis; chronic pancreatitis; pancreatic cancer; pediatric pancreatitis
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Special Issue Information

Dear Colleagues,

Pancreatitis represents a continuum of disorders ranging from an acute episode, to recurrences of acute episodes, to chronic pancreatitis. There are advances in the understanding of the molecular pathogenesis of this continuum of pancreatitis disorders, but there still remains much to be learned, especially in relation to the molecular targets for therapeutic interventions. Importantly, the advances in our understanding of the interplay between cell types of the pancreas, including the influx of myeloid and lymphoid participants that are certainly involved in promoting both the severity of acute pancreatitis and the continuum towards chronic disease, are necessary. The current Special Issue focuses on publishing the scientific research that addresses the advances in the understanding of the intra- and intercellular pathologic mechanisms in the continuum of pancreatitis disorders, with suggestions on how an improved understanding can lead to targets for therapeutic interventions.

Prof. Dr. Stephen J. Pandol
Guest Editor

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Keywords

  • acute pancreatitis
  • chronic pancreatitis
  • recurrent acute pancreatitis
  • inflammatory disorders

Published Papers (1 paper)

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Research

19 pages, 26442 KiB  
Article
Bioinformatic Analyses of Peripheral Blood Transcriptome Identify Altered Neutrophil-Related Pathway and Different Transcriptomic Profiles for Acute Pancreatitis in Patients with and without Chylomicronemia Syndrome
by Chia-Lun Liu and Yang-Hong Dai
Biomolecules 2023, 13(2), 284; https://doi.org/10.3390/biom13020284 - 2 Feb 2023
Viewed by 1779
Abstract
Acute pancreatitis (AP) is a serious inflammatory condition of the pancreas that can be associated with chylomicronemia syndrome (CS). Currently, no study has explored the differences between non-CS-associated AP and CS-associated AP in terms of gene expression. Transcriptomic profiles of blood samples from [...] Read more.
Acute pancreatitis (AP) is a serious inflammatory condition of the pancreas that can be associated with chylomicronemia syndrome (CS). Currently, no study has explored the differences between non-CS-associated AP and CS-associated AP in terms of gene expression. Transcriptomic profiles of blood samples from patients with AP were retrieved from GSE194331 (non-CS-associated) and GSE149607 (CS-associated). GSE31568 was used to examine the linkage between non-CS-associated AP and the expression of micro RNAs (miRNAs). Differentially expressed genes (DEGs) were identified, a gene regulatory network was constructed, and hub genes were defined. Subsequently, single-sample gene set enrichment analysis (ssGSEA) scores of hub genes were calculated to represent their regulatory-level activity. A total of 1851 shared DEGs were identified between non-CS-associated and CS-associated AP. Neutrophils were significantly enriched in both conditions. In non-CS-associated AP, miRNAs including hsa-miR-21, hsa-miR-146a, and hsa-miR-106a demonstrated a lower expression level as compared with the healthy control. Furthermore, the expression patterns and regulatory activities were largely opposite between non-CS-associated and CS-associated AP, with significantly lower estimated neutrophils in the latter case. In summary, we found that the regulation of neutrophils was altered in AP. There was a different gene expression pattern and lower estimated neutrophil infiltration in CS-associated AP. Whether these findings are clinically significant requires further investigation. Full article
(This article belongs to the Special Issue Novel Insights into the Molecular Mechanisms in Pancreatitis)
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