STAT3 and pulmonary fibrosis: In addition to acute injury, JAK2-STAT3 activation also contributed to fibrosis in chronic inflammatory lung diseases (e.g., idiopathic pulmonary fibrosis and interstitial lung disease) by promoting proliferation, senescence, autophagy, endoplasmic reticulum stress, and epithelial/fibroblast to mesenchymal transition (53).