mRNA vaccines take advantage of the mechanism that our cells use to produce proteins. Our cells produce proteins based on the knowledge contained in our DNA; each gene encodes a unique protein. The genetic information is essential, but cells cannot use it until mRNA molecules convert it into instructions for producing specific proteins. mRNA vaccinations provide ready-to-use mRNA instructions for constructing a specific protein. BNT162b2 (Pfizer-BioNTech) and mRNA-1273 (Moderna) both are newly approved mRNA-based COVID-19 vaccines that have shown excellent protection and efficacy. In total, there are five more mRNA-based vaccine candidates for COVID-19 under different phases of clinical development. This review is specifically focused on mRNA-based vaccines for COVID-19 covering its development, mechanism, and clinical aspects.

BackgroundCancer cachexia is a debilitating syndrome associated with marked body loss because of muscular atrophy and fat loss. There are several mechanisms contributing to the pathogenesis of cachexia. The presence of the tumor releases cytokines from inflammatory and immune cells, which play a significant role in activating and deactivating certain pathways associated with protein, carbohydrate, and lipid metabolism. This review focuses on various cascades involving an imbalance between protein synthesis and degradation in the skeletal muscles.ObjectivesThis study aimed to elucidate the mechanisms involved in skeletal muscle wasting phenomenon over the last few years.MethodsThis article briefly overviews different pathways responsible for muscle atrophy in cancer cachexia. Studies published up to April 2023 were included. Important findings and study contributions were chosen and compiled using several databases including PubMed, Google Scholar, Science Direct, and ClinicalTrials.gov using relevant keywords.ResultsCancer cachexia is a complex disease involving multiple factors resulting in atrophy of skeletal muscles. Systemic inflammation, altered energy balance and carbohydrate metabolism, altered lipid and protein metabolism, and adipose tissue browning are some of the major culprits in cancer cachexia. Increased protein degradation and decreased protein synthesis lead to muscle atrophy. Changes in signaling pathway like ubiquitin‐proteasome, autophagy, mTOR, AMPK, and IGF‐1 also lead to muscle wasting. Physical exercise, nutritional supplementation, steroids, myostatin inhibitors, and interventions targeting on inflammation have been investigated to treat cancer cachexia. Some therapy showed positive results in preclinical and clinical settings, although more research on the efficacy and safety of the treatment should be done.ConclusionMuscle atrophy in cancer cachexia is the result of multiple complex mechanisms; as a result, a lot more research has been done to describe the pathophysiology of the disease. Targeted therapy and multimodal interventions can improve clinical outcomes for patients.