Autophagy, a catabolic process, degrades damaged and defective cellular materials through lysosomes, thus working as a recycling mechanism of the cell. It is an evolutionarily conserved and highly regulated process that plays an important role in maintaining cellular homeostasis. Autophagy is constitutively active at the basal level; however, it gets enhanced to meet cellular needs in various stress conditions. The process involves various autophagy-related genes that ultimately lead to the degradation of targeted cytosolic substrates. Many factors modulate both upstream and downstream autophagy pathways like nutritional status, energy level, growth factors, hypoxic conditions, and localization of p53. Any problem in executing autophagy can lead to various pathological conditions including neurodegeneration, aging, and cancer. In cancer, autophagy plays a contradictory role; it inhibits the formation of tumors, whereas, during advanced stages, autophagy promotes tumor progression. Besides, autophagy protects the tumor from various therapies by providing recycled nutrition and energy to the tumor cells. Autophagy is stimulated by tumor suppressor proteins, whereas it gets inhibited by oncogenes. Due to its dynamic and dual role in the pathogenesis of cancer, autophagy provides promising opportunities in developing novel and effective cancer therapies along with managing chemoresistant cancers. In this article, we summarize different strategies that can modulate autophagy in cancer to overcome the major obstacle, i.e., resistance developed in cancer to anticancer therapies.

Conclusion: Carotid interventions affect cognitive function. Summary: Patients experience cognitive decline with aging. Postoperative cognitive decline is observed in patients undergoing surgical procedures. Patients with severe carotid atherosclerotic disease may be at the highest risk of cognitive impairment. Studies have detected cognitive decline in a significant amount of patients who undergo carotid artery interventions including both carotid endarterectomy and carotid artery stenting (Zhou W et al,

Over the past two decades, with advancement of medical research and technology, treatments of many diseases including chronic disorders like rheumatoid arthritis (RA) have been revolutionized. Treatment and management of RA has been refined by advances in understanding its pathologic mechanisms, the development of drugs which target them and its association with various other chronic comorbidities like diabetes. Diabetes prevalence is closely associated with RA since elevated insulin resistance have been observed with RA. It is also associated with inflammation caused due to pro-inflammatory cytokines like tumour necrosis factor α and interleukin 6. Inflammation encourages insulin resistance and also stimulates other factors like a high level of rheumatoid factor in the blood leading to positivity of rheumatoid factor in RA patients. The degree of RA inflammation also tends to influence the criticality of insulin resistance, which increases with high activity of RA and vice versa. Markers of glucose metabolism appear to be improved by DMARDs like methotrexate, hydroxychloroquine, interleukin 1 antagonists and TNF antagonist while glucocorticoids adversely affect glycemic control especially when administered chronically. The intent of the present review paper is to understand the association between RA, insulin resistance and diabetes; the degree to which both can influence the other along with the plausible impact of RA medications on diabetes and insulin resistance.

With over a million deaths every year around the world, lung cancer is found to be the most recurrent cancer among all types. Nonsmall cell lung carcinoma (NSCLC) amounts to about 85% of the entire cases. The other 15% owes it to small cell lung carcinoma (SCLC). Despite decades of research, the prognosis for NSCLC patients is poorly understood with treatment options limited. First, this article emphasises on the part that tumour microenvironment (TME) and its constituents play in lung cancer progression. This review also highlights the inflammatory (pro- or anti-) roles of different cytokines (ILs, TGF-β, and TNF-α) and chemokine (CC, CXC, C, and CX3C) families in the lung TME, provoking tumour growth and subsequent metastasis. The write-up also pinpoints recent developments in the field of chemokine biology. Additionally, it covers the role of extracellular vesicles (EVs), as alternate carriers of cytokines and chemokines. This allows the cytokines/chemokines to modulate the EVs for their secretion, trafficking, and aid in cancer proliferation. In the end, this review also stresses on the role of these factors as prognostic biomarkers for lung immunotherapy, apart from focusing on inflammatory actions of these chemoattractants.