PDF(Pubmed)
Abstract：
Asthma is one of the main non-communicable chronic diseases and affects a huge portion of the population. It is a multifactorial disease, classified into several phenotypes, being the allergic the most frequent. The pathophysiological mechanism of asthma involves a Th2-type immune response, with high concentrations of allergen-specific immunoglobulin E, eosinophilia, hyperreactivity and airway remodeling. These mechanisms are orchestrated by intracellular signaling from effector cells, such as lymphocytes and eosinophils. Ion channels play a fundamental role in maintaining the inflammatory response on asthma. In particular, transient receptor potential (TRP), stock-operated Ca2+ channels (SOCs), Ca2+-activated K+ channels (IKCa and BKCa), calcium-activated chloride channel (TMEM16A), cystic fibrosis transmembrane conductance regulator (CFTR), piezo-type mechanosensitive ion channel component 1 (PIEZO1) and purinergic P2X receptor (P2X). The recognition of the participation of these channels in the pathological process of asthma is important, as they become pharmacological targets for the discovery of new drugs and/or pharmacological tools that effectively help the pharmacotherapeutic follow-up of this disease, as well as the more specific mechanisms involved in worsening asthma.
摘要：
哮喘是主要的非传染性慢性疾病之一，影响着很大一部分人口。这是一种多因素疾病，分为几种表型，过敏最常见。哮喘的病理生理机制涉及Th2型免疫反应，高浓度的过敏原特异性免疫球蛋白E，嗜酸性粒细胞增多,高反应性和气道重塑。这些机制是由效应细胞的细胞内信号协调的，如淋巴细胞和嗜酸性粒细胞。离子通道在维持哮喘的炎症反应中起着基本作用。特别是,瞬时受体电位（TRP），股票运营的Ca2+通道(SOC)，Ca2+激活的K+通道（IKCa和BKCa），钙激活氯离子通道（TMEM16A），囊性纤维化跨膜传导调节因子（CFTR），压电型机械敏感离子通道组分1(PIEZO1)和嘌呤能P2X受体(P2X)。认识到这些通道参与哮喘的病理过程,因为它们成为发现新药和/或药理工具的药理靶标，可以有效地帮助这种疾病的药物治疗随访，以及与哮喘恶化有关的更具体的机制。
