关键词: Gastric precancerous lesions (PLGC) Helicobacter pylori (Hp) Molecular targets Regulatory mechanisms

Mesh : Humans Stomach Neoplasms / pathology drug therapy metabolism Precancerous Conditions / pathology drug therapy Animals Autophagy / drug effects Gastric Mucosa / pathology drug effects metabolism Apoptosis / drug effects Tumor Microenvironment / drug effects Molecular Targeted Therapy Bile Acids and Salts / metabolism Antineoplastic Agents / therapeutic use pharmacology

来  源:   DOI:10.1016/j.biopha.2024.117068

Abstract:
Precancerous lesions of gastric cancer (PLGC) represent a critical pathological stage in the transformation from normal gastric mucosa to gastric cancer (GC). The global incidence of PLGC has been rising over the past few decades, with a trend towards younger onset ages. Increasing evidence suggests that early prevention and treatment of PLGC can effectively reverse the malignant development of gastric mucosal epithelial cells. However, there is currently a lack of effective therapeutic drugs and methods. Recent years have witnessed substantial advancements in PLGC research, with the elucidation of novel regulatory mechanisms offering promising avenues for clinical intervention and drug development. This review aims to delineate potential targets for early prevention and diagnosis of GC while exploring innovative approaches to PLGC management. This article focuses on elucidating the regulatory mechanisms of the inflammatory microenvironment, bile acids (BA), glycolysis, autophagy, apoptosis, ferroptosis, and cellular senescence. We pay particular attention to potential therapeutic targets for PLGC, with the goal of providing insights and theoretical basis for clinical research on PLGC.
摘要:
胃癌癌前病变(PLGC)是正常胃粘膜向胃癌(GC)转变的关键病理阶段。在过去的几十年中,PLGC的全球发病率一直在上升,发病年龄趋于年轻化。越来越多的证据表明,早期预防和治疗PLGC可以有效逆转胃粘膜上皮细胞的恶性发展。然而,目前缺乏有效的治疗药物和方法。近年来,PLGC研究取得了重大进展,随着新型调节机制的阐明,为临床干预和药物开发提供了有希望的途径。这篇综述旨在描述早期预防和诊断GC的潜在目标,同时探索PLGC管理的创新方法。本文着重阐明炎症微环境的调节机制,胆汁酸(BA),糖酵解,自噬,凋亡,铁性凋亡,和细胞衰老。我们特别关注PLGC的潜在治疗靶点,目的是为PLGC的临床研究提供见解和理论依据。
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