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Abstract：
Asthma and chronic obstructive pulmonary disease (COPD) represent chronic inflammatory respiratory disorders that, despite having distinct pathophysiological underpinnings, both feature airflow obstruction and respiratory symptoms. A critical component in the pathogenesis of each condition is the transforming growth factor-β (TGF-β), a multifunctional cytokine that exerts varying influences across these diseases. In asthma, TGF-β is significantly involved in airway remodeling, a key aspect marked by subepithelial fibrosis, hypertrophy of the smooth muscle, enhanced mucus production, and suppression of emphysema development. The cytokine facilitates collagen deposition and the proliferation of fibroblasts, which are crucial in the structural modifications within the airways. In contrast, the role of TGF-β in COPD is more ambiguous. It initially acts as a protective agent, fostering tissue repair and curbing inflammation. However, prolonged exposure to environmental factors such as cigarette smoke causes TGF-β signaling malfunction. Such dysregulation leads to abnormal tissue remodeling, marked by excessive collagen deposition, enlargement of airspaces, and, thus, accelerated development of emphysema. Additionally, TGF-β facilitates the epithelial-to-mesenchymal transition (EMT), a process contributing to the phenotypic alterations observed in COPD. A thorough comprehension of the multifaceted role of TGF-β in asthma and COPD is imperative for elaborating precise therapeutic interventions. We review several promising approaches that alter TGF-β signaling. Nevertheless, additional studies are essential to delineate further the specific mechanisms of TGF-β dysregulation and its potential therapeutic impacts in these chronic respiratory diseases.
摘要：
哮喘和慢性阻塞性肺疾病（COPD）代表慢性炎症性呼吸系统疾病，尽管有不同的病理生理基础，两者都有气流阻塞和呼吸道症状。每种疾病的发病机理中的关键组成部分是转化生长因子-β（TGF-β），一种多功能细胞因子，对这些疾病产生不同的影响。在哮喘中，TGF-β显著参与气道重塑,以上皮下纤维化为标志的一个关键方面，平滑肌肥大，增强粘液的产生，和抑制肺气肿的发展。细胞因子促进胶原沉积和成纤维细胞的增殖，这对气道内的结构改造至关重要。相比之下,TGF-β在COPD中的作用较为模糊。它最初充当保护剂，促进组织修复和抑制炎症。然而,长期暴露于环境因素如香烟烟雾会导致TGF-β信号传导障碍。这种失调导致异常的组织重塑，以过度的胶原蛋白沉积为标志，扩大空域,and,因此，加速发展的肺气肿。此外,TGF-β促进上皮-间质转化（EMT），导致COPD中观察到的表型改变的过程。全面了解TGF-β在哮喘和COPD中的多方面作用对于制定精确的治疗干预措施至关重要。我们回顾了几种改变TGF-β信号传导的有希望的方法。然而，更多的研究对于进一步描述TGF-β失调的具体机制及其在这些慢性呼吸系统疾病中的潜在治疗作用至关重要.
