Department of Medical Laboratory Sciences, Al-Mustaqbal University College, Hilla, Iraq.
Department of Clinical and Laboratory Sciences, College of Pharmacy, University of Al-Qadisiyah, Al-Diwaniyah, Iraq.
Fundam Clin Pharmacol. 2023 Oct;37(5):910-917. doi: 10.1111/fcp.12894. Epub 2023 Apr 2.
Inflammatory bowel disease (IBD) is a chronic life-limiting disease of gastrointestinal tract characterized by widespread enteric inflammation. IBD is a multifactorial disease, and different environmental, microbial, and immune-related factors give rise to the development of disease. Among several factors, the preponderance of pro-inflammatory T helper 17 cells over the anti-inflammatory regulatory T cells augments inflammation in the intestinal mucosa. Prevailing evidence accentuates that PI3K signaling pathway plays a central role in the pathophysiology of the condition by regulating the inflammatory process in the gut mucosa. By recognizing the implications of PI3K in the pathogenesis of IBD, agents that could modulate this pathway have recently been at the focus of research, yielding encouraging results mainly in the experimental IBD models. In this review, we have summarized the recent advances, which may hold the keys to identify novel therapeutic strategies for IBD.
炎症性肠病（IBD）是一种慢性、限制生命的胃肠道疾病，其特征是广泛的肠道炎症。IBD 是一种多因素疾病，不同的环境、微生物和免疫相关因素导致疾病的发展。在几个因素中，促炎辅助性 T 细胞 17 细胞（Th17）超过抗炎调节性 T 细胞（Treg）的优势加剧了肠道黏膜的炎症。现有的大量证据强调，PI3K 信号通路通过调节肠道黏膜中的炎症过程，在该疾病的病理生理学中发挥核心作用。通过认识到 PI3K 在 IBD 发病机制中的作用，最近能够调节该通路的药物成为研究的焦点，主要在实验性 IBD 模型中取得了令人鼓舞的结果。在这篇综述中，我们总结了最近的进展，这些进展可能为 IBD 确定新的治疗策略提供了关键线索。
