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.

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Introduction Oxidative stress (OS) and inflammation are closely related with cancer progression and neurodegenerative diseases. Excess ROS generated either oxidize biomolecules or triggers the signaling cascade thereby activating inflammation. The activation of inflammation causes immune cells to secrete cytokines and chemokines which recruits various immune cells to the site of infection or oxidative stress. This interrelation between oxidative stress and inflammation in cancer and neurodegenerative diseases is discussed in the article. Methods The role of oxidative stress and inflammation in cancer progression and neurodegenerative disease related literature were collected to obtain data. A narrative review was constructed after obtaining all the relevant information to provide a detailed note on it. Results In cancer, OS and inflammation aids in various oncogenic metabolic events including proliferation, differentiation, angiogenesis, migration, invasion, metabolic changes and evading programmed cell death. The disproportion between reactive oxygen species (ROS) and antioxidants in the body is termed as OS which damages the macromolecules (nucleic acids, lipids and proteins). It leads to dysfunction in biological signaling cascade. Prolonged oxidative stress triggers inflammation by stimulating transcription factors (NF-κB, p53, HIF-1α, PPAR-γ, Nrf2, AP-1) which altered expression of various other genes and proteins such as growth factors, tumor suppressor genes, oncogenes, pro-inflammatory cytokines etc., triggering cancer cells survival. In neurodegenerative diseases, both OS and inflammation activates astrocytes and microglia, which in turn altered energy metabolism, proteostasis and redox signaling in brain by activating various protein kinases. Conclusion The present review article delineates the complex interplay between OS and inflammation in some cancers (Colorectal, breast and lung cancer) and neurodegenerative diseases (Alzheimer’s and Parkinson’s disease).