急性呼吸窘迫综合征（acute respiratory distress syndrome，ARDS）是由肺内和肺外病因引发的一种严重的、以顽固性低氧血症为显著特征的呼吸系统危重症，起病较急，发病率和死亡率较高。随着全球范围内的呼吸道病毒的流行和变异，ARDS的诊疗也变得更加复杂，因此临床上亟待探索有关ARDS发生发展的分子机制和有效的治疗方法。研究发现，ARDS的发病机制涉及炎症反应及氧化还原反应失衡、内皮细胞功能失调、肺泡毛细血管屏障的破坏、凝血功能异常等多个因素的相互作用。虽然基因组学、蛋白质组学等分子生物学技术的发展已为ARDS的发病机制提供了全新视角，但仍缺乏早期诊断ARDS的生物标志物和针对性治疗ARDS的有效药物。目前，越来越多的研究表明，瞬时受体电位香草酸亚型1（transient receptor potential vanilloid-1，TRPV1；即辣椒素受体）广泛分布于上呼吸道、气道平滑肌、肺泡和肺血管等部位，参与调解气道舒张和收缩、咳嗽反射、炎症和疼痛相关的炎症介质释放，以及呼吸系统对温度、化学物质和机械牵拉等刺激的感知并传递各种生物信号，在呼吸系统疾病中扮演着重要角色，且已成为肺炎、肺水肿、咳嗽、哮喘、急性肺损伤等呼吸系统疾病的研究热点。基于此，该文以脓毒症、创伤性脑损伤和呼吸道病毒引发的ARDS与TRPV1的相关性和分子机制为切入点进行综述，总结了调控TRPV1的表达对ARDS发病进程所发挥的积极作用，旨在为加强ARDS的早期诊断和有效干预措施提供参考。

Acute respiratory distress syndrome (ARDS) is a severe critical respiratory disease characterized by refractory hypoxemia, which is caused by intrapulmonary and extrapulmonary factors. It has a rapid onset, and high morbidity and mortality. With the global prevalence and mutation of respiratory viruses, the diagnosis and treatment of ARDS have become more complicated, requiring exploration into the molecular mechanisms and effective therapeutic methods of the occurrence and development of ARDS in clinical practice. Researchers have found that the pathogenesis of ARDS involves the interaction of multiple factors, including imbalances in inflammatory responses and redox reactions, dysregulation of endothelial cells, disruption of alveolar-capillary barrier and abnormalities in coagulation function. Although advancements in molecular biology techniques such as genomics and proteomics have provided new insights into the pathogenesis of ARDS, there is still a lack of early diagnostic biomarker and effective drugs targeted for ARDS. At present, more comprehensive and in-depth basic and clinical research is still needed. Increasing evidence suggests that transient receptor potential vanilloid-1 (TRPV1), also known as the capsaicin receptor, plays a crucial role in respiratory system diseases. TRPV1 is widely distributed in the upper respiratory tract, airway smooth muscle, alveoli and pulmonary blood vessels, participating in mediating airway dilation and constriction, cough reflex, and release of inflammatory mediators related to inflammation and pain, as well as sensing and transmitting various biological signals related to temperature, chemical substances and mechanical stress stimuli in the respiratory system. The widespread distribution and diverse physiological functions of TRPV1 make it a research hotspot in the occurrence and development of respiratory system diseases such as pneumonia, pulmonary edema, cough, asthma and acute lung injury. This article reviews the correlation and molecular mechanisms between ARDS caused by sepsis, traumatic brain injury and respiratory viruses with TRPV1, aiming to summarize the positive effects of regulating TRPV1 expression on the pathogenesis of ARDS and provide reference for strengthening early diagnosis and effective intervention measures for ARDS.