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Study type | Model/sample | Impact on PTEN | Additional signaling | Biological process | Ref. |
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In vivo/in vitro | Emphysema mouse model; bone marrow–derived macrophages (BMDMs); CSE-treated RAW264.7 and L929 cell lines | Decreased PTEN expression | Activated the PI3K/Akt pathway | Macrophage polarization toward the M2 phenotype in COPD | [75] |
In vivo/in vitro | CS-exposed mouse model; BEAS-2B cells | Increased PTEN stability | Inhibited the PI3K/Akt pathway, decreased PRMT6 expression, promoted PI3Kp85 expression, and inhibited PDK1 | Resulted in epithelial cell death in COPD | [76] |
In vivo | Human lung tissue of COPD | Decreased PTEN expression | Activated HIF-1α signaling and MMP7/9 | Decreased levels of oxidases (LOX, LOXL1, and LOXL2) caused abnormalities in elastic fiber biology | [77–79] |
In vitro | CSE-exposed BEAS-2B cells | PTEN oxidation | Increased p-Akt level | Impaired Trx-1 activity | [80] |
In vivo/in vitro | Lung tissues of patients with COPD; cells collected from patients undergoing lung resection surgery; BEAS-2B cells | Loss of PTEN expression | PI3K/mTOR signaling activation and SIRT1/6 inhibition | Caused cell senescence in COPD | [81, 82] |
In vivo/in vitro | Human peripheral lung tissue; normal human bronchial epithelial cell line (16HEB) | Downregulation of PTEN | Decreased lncRNA SHNG5 sponge miR-132 expression | Regulated effects of CSE on cell proliferation, apoptosis, and inflammation | [84] |
In vivo | Patients with COPD | Decreased PTEN expression | Enhanced the STAT3-AP-1 interaction | Increased MMP-9 expression to regulate airway remodeling | [87] |
In vitro | Mouse cardiac endothelial cells (MCECs) | Low expression of PTEN | ROS/Src/EGFR-p38MAPK pathway | PTEN pathway related with AJC transcriptional reprograming to regulate epithelial barrier | [78, 90] |
In vitro | Human nasal epithelial cell line (RPMI 2650) | Reduced PTEN activity | Increased TLR4/JNK/Bnip3 signaling | Activated mitophagy and induced mitochondrial dysfunction to cause epithelial cell apoptosis, proliferation arrest, and migration inhibition | [91] |
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