Emerging trends in the novel drug delivery approaches for the treatment of lung cancer

Abstract

Cancer is one of the major diseases that cause a high number of deaths globally. Of the major types of cancers, lung cancer is known to be the most chronic form of cancer in the world. The conventional management of lung cancer includes different medical interventions like chemotherapy, surgical removal, and radiation therapy. However, this type of approach lacks specificity and also harms the adjacent normal cells. Lately, nanotechnology has emerged as a promising intervention in the management and treatment of lung cancers. Nanotechnology has revolutionized the existing modalities and focuses primarily on reducing toxicity and improving the bioavailability of anticancer drugs to the target tumor cells. Nanocarrier systems are being currently used extensively to exploit and to overcome the obstructions induced by cancers in the lungs. The nano-carrier-loaded therapeutic drug delivery methods have shown promising potential in treating lung cancer as its target is to control the growth of tumor cells. In this review, various modes of nano drug delivery options like liposomes, dendrimers, quantum dots, carbon nanotubes and metallic nanoparticles have been discussed. Nano-carrier drug delivery systems emerge as a promising approach and thus is expected to provide newer and advanced avenues in cancer therapeutics.

Wogonin ameliorate complete Freund's adjuvant induced rheumatoid arthritis via targeting NF‐κB/MAPK signaling pathway

“…In RA, by secreting proinflammatory cytokines and mediators that drive angiogenesis, immune cell infiltration, and cartilage and bone destruction, macrophages are the key effector cells in the acute and chronic phases . The amount of macrophages in the inflamed synovium increases owing to development of resident macrophages and infiltration through flowing monocytes . Recent surveys indicate that mitogen‐activated protein kinases (MAPKs) in macrophages are extremely activated and engaged in RA pathogenesis .…”

“…7 The amount of macrophages in the inflamed synovium increases owing to development of resident macrophages and infiltration through flowing monocytes. 8,9 Recent surveys indicate that mitogen-activated protein kinases (MAPKs) in macrophages are extremely activated and engaged in RA pathogenesis. 10 Many organizations have focused on blocking intracellular nuclear factor-κB (NF-κB) and p38 MAPK signaling pathways to discover a new generation of anti-inflammatory medicines for RA.…”

Molecular signaling of G‐protein‐coupled receptor in chronic heart failure and associated complications

“…In addition, both the active biological peptide that is, Ang II mediates cell proliferation, aldosterone release, fibrosis, vasoconstriction, and inflammatory effects via AT1 Receptor in chronic HF and Ang 1‐7 have counter‐regulatory effects via Mas Receptor (Romero, Orias, & Weir, ). The vasoconstrictive response of AT1 stimulation leads to an increase in the preload and afterload of failing stress heart (Sharma et al, ; Singh et al, ). Moreover, the release of aldosterone from adrenal cortex in response to volume depletion causes fibrosis and hypertrophy of cardiac system.…”

“…mediates cell proliferation, aldosterone release, fibrosis, vasoconstriction, and inflammatory effects via AT1 Receptor in chronic HF and Ang 1-7 have counter-regulatory effects via Mas Receptor (Romero, F I G U R E 1 Heart failure pathophysiology of stimulated compensatory sympathetic activity mediated beta receptor and angiotensin receptor overstimulation and its biological response F I G U R E 2 Counter balance of cardiac activity of RAAS in normal physiology Orias, & Weir, 2015). The vasoconstrictive response of AT1 stimulation leads to an increase in the preload and afterload of failing stress heart(Sharma et al, 2019;Singh et al, 2017). Moreover, the release of aldosterone from adrenal cortex in response to volume depletion causes fibrosis and hypertrophy of cardiac system.…”

Sjogren‐Larsson syndrome associated hypermelanosis

“…The MC1R agonists α‐MSH and ACTH stimulate the formation of eumelanin While the synthesis of pheomelanin is performed by the stimulating protein agonist (ASP) . However, it was thought that α‐melanocyte stimulating hormone (α‐MSH) was the primary ligand for this receptor and was found in the pituitary and proopiomelanocortin (POMC) gene product.…”