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Your search keyword '"Cicchinelli, Sara"' showing total 2 results
Start Over Author "Cicchinelli, Sara" Topic inflammatory bowel disease
2 results on '"Cicchinelli, Sara"'

1. Intestinal Fibrogenesis in Inflammatory Bowel Diseases: Exploring the Potential Role of Gut Microbiota Metabolites as Modulators.

Author

Cicchinelli, Sara, Gemma, Stefania, Pignataro, Giulia, Piccioni, Andrea, Ojetti, Veronica, Gasbarrini, Antonio, Franceschi, Francesco, and Candelli, Marcello

Subjects
*INFLAMMATORY bowel diseases, *GUT microbiome, *INTESTINES, *PATHOLOGICAL physiology, *EPITHELIAL-mesenchymal transition
Abstract

Fibrosis, sustained by the transformation of intestinal epithelial cells into fibroblasts (epithelial-to-mesenchymal transition, EMT), has been extensively studied in recent decades, with the molecular basis well-documented in various diseases, including inflammatory bowel diseases (IBDs). However, the factors influencing these pathways remain unclear. In recent years, the role of the gut microbiota in health and disease has garnered significant attention. Evidence suggests that an imbalanced or dysregulated microbiota, along with environmental and genetic factors, may contribute to the development of IBDs. Notably, microbes produce various metabolites that interact with host receptors and associated signaling pathways, influencing physiological and pathological changes. This review aims to present recent evidence highlighting the emerging role of the most studied metabolites as potential modulators of molecular pathways implicated in intestinal fibrosis and EMT in IBDs. These studies provide a deeper understanding of intestinal inflammation and fibrosis, elucidating the molecular basis of the microbiota role in IBDs, paving the way for future treatments. [ABSTRACT FROM AUTHOR]

Published
2024
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2. DDS-induced colorectal fibrosis in mice: anti-fibrotic effects of GED 0507-34 levo, a novel PPARγ ligand

Author

Pompili, Simona, Sferra, Roberta, Vetuschi, Antonella, Latella, Giovanni, Gaudio, Eugenio, Cicchinelli, Sara, and Speca, Silvia

Subjects
Inflammatory Bowel Disease, animal model, fibrosis, TGFβ/Smads, PPARγ, digestive system diseases
Abstract

Intestinal fibrosis is a progressive process characterized by de novo synthesis and uncontrolled deposition of extracellular matrix components (ECM) following a tissue chronic inflammation mainly regulated by Transforming Growth Factor (TGF)β/ Smads pathway. Frequently associated to Inflammatory Bowel Disease (IBD), intestinal fibrosis may lead to stenosis and obstructions that require surgery up to 75% of patients as drugs currently used in IBD are unable to improve fibrostenosis lesions (1). Peroxisome proliferator-activated receptor (PPAR)-γ is able to antagonize (TGF) β/Smads and could be an crucial target to develop novel antifibrotic therapeutic strategies (2). Aim of this study is to evaluate the antifibrotic action of a novel PPARγ agonist, GED 0507-34 levo, in colonic fibrosis in mice. Immunohistochemistry and immunoblotting evaluations, TGFβ1, CTGF, Collagen types I-III, Smad3, α-SMA, were performed in in three groups of C57BL/6 mice: Dextran Sulphate Sodium (DSS) colitis group, DSS+GED group and controls. Evident macroscopic and microscopic lesions in the most of colons of DSS treated mice were observed compared to DSS+GED mice and controls. The tissue levels of the main markers of fibrosis resulted significantly increased in DSS mice and restored by administration of GED. GED seems to prevents ECM colonic deposition and to improve the intestinal fibrotic lesions by its ability in controlling TGFβ/Smads pathway signalling activation., Italian Journal of Anatomy and Embryology, Vol 119, No 1 (Supplement) 2014

Published
2015
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