שמור ב:
| Main Authors: | , , , |
|---|---|
| פורמט: | Recurso digital |
| שפה: | אנגלית |
| יצא לאור: |
Zenodo
2025
|
| נושאים: | |
| גישה מקוונת: | https://doi.org/10.5281/zenodo.14870932 |
| תגים: |
הוספת תג
אין תגיות, היה/י הראשונ/ה לתייג את הרשומה!
|
תוכן הענינים:
- <p><strong><span>Abstract: </span></strong><span>The intestinal barrier constitutes the largest surface of the human body communicating with the external environment. As a complex system, it developed numerous mechanisms allowing the organism to interact with various stimuli, such as residual microbiome. Alterations affecting elements of intestinal wall may lead to increased intestinal permeability and resulting translocation of bacteria or its components to the bloodstream in the form of the “leaky gut syndrome” (LGS). One of the most common causes of LGS is the disruption of tight junctions (TJ) maintained by tight junction proteins (TJP). LGS and associated alterations in TJP are observed in numerous gastrointestinal (GI) diseases characterized by chronic and relapsing inflammation affecting the GI tract, including inflammatory bowel diseases (IBD) such as </span><span>Crohn’s disease</span><span> (CD) and ulcerative colitis (UC)<span>. Current literature indicates the key role of LGS in many pathological processes further emphasizing the need for effective pharmacological approaches to treat this syndrome. One of the potential pharmacological targets in LGS treatment are members of the cytochrome P450 (CYP450) superfamily responsible for the metabolism of various endo- and exogenous compounds. Recent studies show that CYP450s are involved in the pathophysiology of the GI by influencing inflammation and intestinal barrier function. This review summarizes the findings on the role of CYP450 isoforms in intestinal hyperpermeability and their potential involvement in the pathophysiology of LGS.</span></span></p>