Ding Changhui, Gai Senxi, Ma Zhiyong, Yang Lizhuo, Fu Zhijie
Department of Otorhinolaryngology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Jinan, China.
The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China.
Front Pharmacol. 2024 Jul 1;15:1431330. doi: 10.3389/fphar.2024.1431330. eCollection 2024.
Chronic sinusitis is a common inflammatory disease of the nasal and sinus mucosa, leading to symptoms such as nasal congestion, runny nose, decreased sense of smell, and headache. It often recurs and seriously affects the quality of life of patients. However, its pathological and physiological mechanisms are not fully understood. In recent years, the role of potassium ion channels in the regulation of mucosal barrier function and inflammatory cell function has received increasing attention. In chronic sinusitis, there are often changes in the expression and function of potassium channels, leading to mucosal damage and a stronger inflammatory response. However, the related research is still in its early stages. This article will review the role of the potassium channel in the pathological and physiological changes of chronic sinusitis. The studies revealed that BK/TREK-1 potassium channel play a protective role in the nasal mucosal function through p38-MAPK pathway, and KCa3.1/Kv1.3 enhance the inflammatory response of Chronic rhinosinusitis by regulating immune cell function, intracellular Ca signaling and ERK/MAPK/NF-κB pathway. Because ion channels are surface proteins of cell membranes, they are easier to intervene with drugs, and the results of these studies may provide new effective targets for the prevention and treatment of chronic sinusitis.
慢性鼻窦炎是鼻腔和鼻窦黏膜常见的炎症性疾病,可导致鼻塞、流涕、嗅觉减退和头痛等症状。该病常反复发作,严重影响患者的生活质量。然而,其病理生理机制尚未完全明确。近年来,钾离子通道在调节黏膜屏障功能和炎症细胞功能中的作用日益受到关注。在慢性鼻窦炎中,钾通道的表达和功能常发生改变,导致黏膜损伤和更强的炎症反应。然而,相关研究仍处于早期阶段。本文将综述钾通道在慢性鼻窦炎病理生理变化中的作用。研究表明,BK/TREK-1钾通道通过p38-MAPK途径对鼻黏膜功能起保护作用,而KCa3.1/Kv1.3通过调节免疫细胞功能、细胞内钙信号和ERK/MAPK/NF-κB途径增强慢性鼻窦炎的炎症反应。由于离子通道是细胞膜的表面蛋白,更容易受到药物干预,这些研究结果可能为慢性鼻窦炎的防治提供新的有效靶点。