Table 1.
Respiratory Disease | Therapy | CS-Induced Mechanism | Reference |
---|---|---|---|
COPD | Metformin | Inhibition of apoptosis through regulation of AMP kinase. | [226] |
Astaxanthin | Inhibition of Nrf2-modulated oxidative stress and regulation of NF-κB-related inflammatory responses through binding with SIRT1. | [231] | |
HUC-MSC- derived EVs |
Alleviation of airway inflammation in the CS-induced rat model. | [232] | |
LPHNPs | Upregulation of cytocompatibility toward bronchial epithelial cells and macrophages. | [233] | |
Pulmonary Fibrosis |
N-acetylcysteine | Replenish the levels of the antioxidant glutathione and reduce reactive oxygen species by targeting pro-inflammatory cytokines such as TNF-α, IL-1, and TGF-β. | [262,263] |
PDE4B inhibitors | Reducing inflammation and fibrotic processes by inhibiting the degradation of cAMP. | [269] | |
Cancer | PD-1/PD-L1 inhibitors | Enhance the immune system’s ability to target cancer cells and restore immune cell functionality by combining PD-L1 from cancer and PD-1 from T cells. | [309] |
Trastuzumab | Durable anticancer activity in patients with previously treated HER2-mutant of NSCLC. | [291] | |
Rituximab | Depletes CD20-positive B cells in lung tumors. | [292] | |
CRISPR-Cas9 | Modify or correct disease-related genes causing mutations in cancer cells. | [316] | |
CAR-T-cell | improve the survival and functionality of engineered T-cells by reducing ROS and eliminating cancer cells. | [318] | |
MSCs-exosome | Cell-to-cell communication within the tumor microenvironment and suppression of angiogenesis. | [321] | |
ARDS and AE-COPD |
Vitamin C | Antioxidant vitamin C inhibits ROS-mediated NET by inactivating NADPH oxidase. | [335] |
ICAM/NLC | Decrease pro-inflammatory cytokines in the ARDS mouse model. | [338] |