IPF is a chronic, progressive, and frequently fatal disease associated with aging and dysfunctional autophagy. It is accepted that accelerated epithelial cell senescence plays a vital role in IPF pathogenesis by virtue of atypical epithelial–mesenchymal interactions, and insufficient autophagy is attributed as a mechanism of accelerated epithelial cell senescence and myofibroblast differentiation in IPF [155]. Bleomycin is widely used as a model of drug-induced lung fibrosis. The first study to describe the protective role of autophagy in bleomycin-induced lung fibrosis used the Atg4b-deficient mice model [156]. After 7 days of bleomycin treatment, these mice demonstrated a significantly higher neutrophilic infiltration and inflammatory cytokine production as compared to untreated mice [156]. Additionally, after 28 days of bleomycin treatment, mice developed extensive lung fibrosis, which was accompanied by an elevated collagen deposition and deregulated expression of extracellular matrix genes [156]. Similarly, in mice deficient in LC3B (LC3B−/−), bleomycin-mediated lung injury and fibrotic changes were more pronounced, suggesting the protective role of autophagy in bleomycin-induced lung injury and the resulting development of fibrotic lung disease in mice [157]. Another recent study describes the protective role of the anti-inflammatory cytokine IL-37 in the IPF murine model [158]. A further mechanistic delve into the mechanism of IL-37-mediated protection showed that it induces Beclin-1-dependent autophagy while downregulating TGFβ1-mediated lung fibroblast proliferation [158]. Moreover, IL-37 also decreased inflammation and collagen deposition in bleomycin-treated murine lungs while the protective effect was reversed by treatment with 3-methyladinine (3MA), an autophagy inhibitor [158]. Thus, it is plausible that a decrease in IL-37-mediated autophagy might be involved in the progression of IPF. Moreover, the protective effects of autophagy are apparent from this and the other mechanistic studies mentioned above.