慢性阻塞性肺疾病（COPD）目前是全球发病率和死亡率最高的疾病之一，是一种严重的公共卫生问题。肺动脉高压是COPD的常见并发症。目前，肺动脉高压的发病机制尚不清楚。已知导致COPD患者肺动脉高压的因素包括低氧和炎症。低氧是由于肺损伤和供氧不足导致的，可以引起肺血管收缩和增加血管阻力，从而促进COPD患者肺动脉高压的发展。炎症也在肺动脉高压的进展中起重要作用。COPD患者的肺组织中存在炎症反应，并释放出各种炎症介质。这些介质可以刺激肺动脉内皮细胞和平滑肌细胞的异常增殖，导致血管壁增厚和血流受限。本文重点讨论了四种炎症因子（白介素(IL)-1β、IL-6、IL-8和肿瘤坏死因子(TNF)-α）在肺动脉高压中的发病机制。IL-1β、IL-6、IL-8和TNF-α是已知的促炎细胞因子，在炎症反应中起到重要作用。在肺动脉高压的背景下，这些炎症因子与肺血管重塑有关，导致血管阻力增加和血流受损。本文的研究将深入探讨IL-1β、IL-6、IL-8和TNF-α在肺血管重塑、内皮功能障碍、平滑肌细胞增殖和炎症中的作用。研究的目标是全面介绍它们在肺动脉高压中的参与程度，并探讨这些因素如何受高海拔地区普遍存在的低氧环境影响。通过关注这些炎症因子在高海拔地区的相关性，我们希望为该地区居民提供有价值的见解，以指导临床管理策略、预防措施和潜在治疗干预措施，降低他们患肺动脉高压的风险。

Chronic obstructive pulmonary disease (COPD) is currently one of the highest morbidity and mortality worldwide, a serious public health problem. Pulmonary hypertension is a common complication of COPD. At present, the pathogenesis of pulmonary hypertension is not clear. A concise overview of the known factors contributing to pulmonary hypertension in COPD includes hypoxia and inflammation. Hypoxia, resulting from lung damage and inadequate oxygen supply, can lead to pulmonary vasoconstriction and increased vascular resistance, thus contributing to the development of pulmonary hypertension in COPD patients. Inflammation also plays a significant role in the progression of pulmonary hypertension. COPD patients exhibit inflammatory responses in their lung tissues, with the release of various inflammatory mediators. These mediators can stimulate abnormal proliferation of endothelial cells and smooth muscle cells within the pulmonary arteries, leading to vascular wall thickening and restricted blood flow. This paper focuses on the pathogenesis of four inflammatory factors, namely interleukin (IL-1β), IL-6, IL-8, and tumor necrosis factor (TNF)-α, in pulmonary hypertension. IL-1β, IL-6, IL-8, and TNF-α are known as pro-inflammatory cytokines that play crucial roles in the inflammatory response. In the context of pulmonary hypertension, these inflammatory factors have been implicated in the remodeling of the pulmonary vasculature, leading to increased vascular resistance and impaired blood flow. The research presented in this paper will delve into the current scientific knowledge surrounding IL-1β, IL-6, IL-8, and TNF-α, and their roles in pulmonary vascular remodeling, endothelial dysfunction, smooth muscle cell proliferation, and inflammation. The goal is to provide a comprehensive overview of their involvement in pulmonary hypertension and how these factors may be influenced by the hypoxic environment prevalent in high-altitude regions. By focusing on the relevance of these inflammatory factors in high-altitude areas, we hope to contribute valuable insights that can inform clinical management strategies, prevention approaches, and potential therapeutic interventions for individuals residing in such regions who are at an increased risk of developing pulmonary hypertension.