Activation of the mTOR pathway induces senescence in pulmonary arterial smooth muscle cells and endothelial cells, inhibits the expression of autophagy-related proteins such as LC3, ATG3, and ATG5, and promotes the release of inflammatory cytokines IL-6, IL-8, and CCL2, driving typical pathological changes of COPD, including emphysema, pulmonary arterial hypertension, and chronic inflammation (55). This evidence concerns the gene MAP1LC3A and pulmonary arterial hypertension.