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Abstract：
Chronic obstructive pulmonary disease (COPD), the major leading cause of mortality worldwide, is a progressive and irreversible respiratory condition characterized by peripheral airway and lung parenchymal inflammation, accompanied by fibrosis, emphysema, and airflow limitation, and has multiple etiologies, including genetic variance, air pollution, and repetitive exposure to harmful substances. However, the precise mechanisms underlying the pathogenesis of COPD have not been identified. Recent multiomics-based evidence suggests that the plasticity of alveolar macrophages contributes to the onset and progression of COPD through the coordinated modulation of numerous transcription factors. Therefore, this review focuses on understanding the mechanisms and functions of macrophage polarization that regulate lung homeostasis in COPD. These findings may provide a better insight into the distinct role of macrophages in COPD pathogenesis and perspective for developing novel therapeutic strategies targeting macrophage polarization.
摘要：
慢性阻塞性肺疾病(COPD),全球主要的死亡原因，是一种进行性和不可逆的呼吸系统疾病，其特征是周围气道和肺实质炎症，伴有纤维化，肺气肿,和气流限制，有多种病因，包括遗传变异，空气污染,反复接触有害物质。然而,COPD发病机制的确切机制尚未确定.最近基于多组学的证据表明，肺泡巨噬细胞的可塑性通过多种转录因子的协调调节促进COPD的发生和发展。因此,本文综述了巨噬细胞极化调节COPD肺稳态的机制和功能。这些发现可以更好地了解巨噬细胞在COPD发病机理中的独特作用，并为开发针对巨噬细胞极化的新型治疗策略提供前景。
