In addition, autophagy dysfunction has been now widely accepted as a pathogenic mechanism in IPF, and thus strategies to augment autophagy are justified as relevant potential interventions in controlling IPF pathogenesis [209]. Indeed, some recent studies have shown that autophagy mitigates IPF pathogenesis by regulating the fibroblast apoptosis and senescence of alveolar epithelial cells [209]. Moreover, a recent report describes the utility of IL-37 in reducing the bleomycin-induced inflammation and collagen deposition in murine lungs by increasing Beclin-1-dependent autophagy [158].