Institute of Translational Pharmacology (IFT), National Research Council of Italy (CNR), Section of Palermo, Via Ugo La Malfa 153, 90146 Palermo, Italy.
Biomolecules. 2023 Aug 4;13(8):1217. doi: 10.3390/biom13081217.
Autophagy is the key process by which the cell degrades parts of itself within the lysosomes. It maintains cell survival and homeostasis by removing molecules (particularly proteins), subcellular organelles, damaged cytoplasmic macromolecules, and by recycling the degradation products. The selective removal or degradation of mitochondria is a particular type of autophagy called mitophagy. Various forms of cellular stress (oxidative stress (OS), hypoxia, pathogen infections) affect autophagy by inducing free radicals and reactive oxygen species (ROS) formation to promote the antioxidant response. Dysfunctional mechanisms of autophagy have been found in different respiratory diseases such as chronic obstructive lung disease (COPD) and asthma, involving epithelial cells. Several existing clinically approved drugs may modulate autophagy to varying extents. However, these drugs are nonspecific and not currently utilized to manipulate autophagy in airway diseases. In this review, we provide an overview of different autophagic pathways with particular attention on the dysfunctional mechanisms of autophagy in the epithelial cells during asthma and COPD. Our aim is to further deepen and disclose the research in this direction to stimulate the develop of new and selective drugs to regulate autophagy for asthma and COPD treatment.
自噬是细胞在溶酶体内降解自身部分的关键过程。它通过去除分子（特别是蛋白质）、亚细胞细胞器、受损的细胞质大分子，并回收降解产物，来维持细胞存活和内稳态。线粒体的选择性去除或降解是一种称为自噬的特殊类型的自噬。各种形式的细胞应激（氧化应激（OS）、缺氧、病原体感染）通过诱导自由基和活性氧（ROS）的形成来促进抗氧化反应，从而影响自噬。自噬的功能障碍机制在不同的呼吸系统疾病中已经被发现，如慢性阻塞性肺疾病（COPD）和哮喘，涉及上皮细胞。一些现有的临床批准的药物可以在不同程度上调节自噬。然而，这些药物是非特异性的，目前不用于在气道疾病中操纵自噬。在这篇综述中，我们提供了不同自噬途径的概述，特别关注哮喘和 COPD 期间上皮细胞中自噬的功能障碍机制。我们的目的是进一步深化和揭示这一方向的研究，以刺激开发新的和选择性的药物来调节自噬，以治疗哮喘和 COPD。
