Lung injury is characterized by inflammatory processes demonstrated as loss of function of the pulmonary capillary endothelial and alveolar epithelial cells. Autophagy is an intracellular digestion system that work as an inducible adaptive response to lung injury which is a resultant of exposure to various stress agents like hypoxia, ischemia-reperfusion and xenobiotics which may be manifested as acute lung injury (ALI), acute respiratory distress syndrome (ARDS), chronic lung injury (CLI), bronchopulmonary dysplasia (BPD), chronic obstructive pulmonary disease (COPD), asthma, ventilator-induced lung injury (VILI), ventilator-associated lung injury (VALI), pulmonary fibrosis (PF), cystic fibrosis (CF) and radiation-induced lung injury (RILI). Numerous regulators like LC3B-II, Beclin 1, p62, HIF1/BNIP3 and mTOR play pivotal role in autophagy induction during lung injury possibly for progression/inhibition of the disease state. The present review focuses on the critical autophagic mediators and their potential cross talk with the lung injury pathophysiology thereby bringing to limelight the possible therapeutic interventions.

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Objectives Scopoletin (6-methoxy-7-hydroxycoumarin) is a naturally occurring coumarin belonging to the category of secondary metabolites. Coumarins are commonly found in several herbs and play a prominent role in the defense mechanism of plants. Beneficial effects of scopoletin including antioxidant, anti-diabetic, hepatoprotective, neuroprotective and anti-microbial activity induced via numerous intracellular signalling mechanisms have been widely studied. However, anti-inflammation and anti-tumorigenesis properties of scopoletin are not well documented in the literature. Therefore, the primary focus of the present review was to highlight the plethora of research pertaining to the signalling mechanisms associated with the prevention of the progression of disease condition by scopoletin. Key findings Multiple signalling pathways like nuclear erythroid factor-2 (NEF2)-related factor-2 (NRF-2), apoptosis/p53 signalling, nuclear factor-κB (NF-κB) signalling, autophagy signalling, hypoxia signalling, signal transducer and activator of transcription-3 (STAT3) signalling, Wnt-β signalling, Notch signalling are coupled with the anti-inflammation and anti-tumorigenesis potential of scopoletin. Summary Understanding crucial targets in these molecular signalling pathways may support the role of scopoletin as a promising naturally derived bioactive compound for the treatment of several diseases.