Abstract
COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been considered a public health emergency, extensively investigated by researchers. Accordingly, the respiratory tract has been the main research focus, with some other studies outlining the effects on the neurological, cardiovascular, and renal systems. However, concerning SARS-CoV-2 outcomes on skeletal muscle, scientific evidence is still not sufficiently strong to trace, treat and prevent possible muscle impairment due to the COVID-19. Simultaneously, there has been a considerable amount of studies reporting skeletal muscle damage in the context of COVID-19. Among the detrimental musculoskeletal conditions associated with the viral infection, the most commonly described are sarcopenia, cachexia, myalgia, myositis, rhabdomyolysis, atrophy, peripheral neuropathy, and Guillain-Barré Syndrome. Of note, the risk of developing sarcopenia during or after COVID-19 is relatively high, which poses special importance to the condition amid the SARS-CoV-2 infection. The yet uncovered mechanisms by which musculoskeletal injury takes place in COVID-19 and the lack of published methods tailored to study the correlation between COVID-19 and skeletal muscle hinder the ability of healthcare professionals to provide SARS-CoV-2 infected patients with an adequate treatment plan. The present review aims to minimize this burden by both thoroughly exploring the interaction between COVID-19 and the musculoskeletal system and examining the cutting-edge 3D cell culture techniques capable of revolutionizing the study of muscle dynamics.
Highlights
In December 2019, a novel coronavirus designated as “SARS-CoV-2” emerged in Wuhan, China
The Muscle Impairment COVID-19 3D Culture respiratory tract was established as the main SARS-CoV-2 infection focus and, has been the primary system studied in medical research endeavors
Uncertainty regarding the exact mechanisms that explain the wide range of symptoms and secondary diseases experienced by individuals infected by SARS-CoV-2 has been preventing the medical field from providing adequate treatment to patients
Summary
In December 2019, a novel coronavirus designated as “SARS-CoV-2” emerged in Wuhan, China. An increase in type I interferons is seen in coronavirus infections, due to the fact that IFIH1 augments the production of cytokines such as IFN-γ, IL-1β, TNF-α, IL-6, and IL-18 [86], which would contribute to autoimmune disease emergence This was recently demonstrated in dermatomyositis patients in 2020 which identified six distinct epitopes with high sequence identity to the human SARS-CoV-2 virus. Inflammatory mediators play a causative role in diaphragm dysfunction, due to the activation of proteolytic pathways and an increased amount of neutrophils and macrophages [11] These findings are of critical importance to severely ill SARSCoV-2 infected patients since constantly evaluating mechanical ventilation time could potentially contribute to reducing COVID-19’s detrimental effects on patients. It is due to this endogenous remodeling capability that fibrin is commonly applied in skeletal muscle modeling and tissue engineering endeavors, as muscle cells are able to degrade and replace the base fibrin scaffold with naturally secreted ECM [165]
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