Table 1. The key molecules involved in regulating autophagy and ferroptosis.

Molecules	Functional mechanism in PF	Targeted drugs
Abbreviations: AMPK, AMP-activated protein kinase; ECM, extracellular matrix; EMT, epithelial-mesenchymal transition; GPX4, glutathione peroxidase 4; GSH, glutathione; KEAP1, Kelch-like ECH-associated protein 1; mTORC1, mechanistic target of rapamycin complex 1; NRF2, nuclear factor erythroid 2-related factor 2; p62/SQSTM1, sequestosome-1; PF, pulmonary fibrosis; ROS, reactive oxygen species; SLC7A11, solute carrier family 7 member 11; TGF-β1, transforming growth factor-beta 1.
NRF2	Inhibit the TGF-β1/Smad pathway, collagen deposition, antioxidant, and anti-inflammatory[62]	Activator: Rapamycin[63], Tanshinone ⅡA[64], Rosavin[65]
KEAP1	Promote NRF2 degradation and disrupt its imbalance, regulate cell proliferation and collagen deposition[66]	Inhibitor: Bardoxolone-methyl[67], Sinomenine[68]
p62/SQSTM1	Facilitate autophagosome formation, regulate iron metabolism and TGF-β/Smad pathway[69]	Inhibitor: Bergenin[70], Protodioscin[71]
mTORC1/AMPK	Regulate ECM production, involve the secretion of pro-inflammatory factors[72]	Inhibitor: Omipalisib[73], Rapalogs[74], Everolimus[75]
GPX4	Regulate autophagy and ferroptosis, block fibroblast activation and suppress EMT[76]	GPX4-inactivating agent: FINO2[77], RSL3[78]
SLC7A11	Promote cystine uptake and GSH synthesis, thereby enhancing antioxidant capacity and suppressing ferroptosis[79]	Activator: Sulforaphane[80] Inhibitor: Erastin[81], Sorafenib[82]