Emerging evidence suggests multiple mechanisms underlying CH’s protective effects: inhibition of NF-κB signaling in LPS-induced endotoxin shock [34], activation of the Nrf2/ARE pathway in bleomycin-induced pulmonary fibrosis [35], and modulation of the AMPK/mTOR/ULK-1 axis in rheumatoid arthritis fibroblast-like synoviocytes [16]. Here, ULK1 is linked to pulmonary fibrosis.