Abdulrahim Abu Jayyab
Individual infected with the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), though the clinical presentation ranges from asymptomatic to mild flu-like symptoms, a significant minority develop severe lung injury with pneumonia, acute respiratory distress syndrome (ARDS) , respiratory failure, systemic inflammation, and multiorgan failure, which leading to considerable morbidity and mortality in the majority of the elderly patients with previous cardiovascular and chronic pulmonary inflammation comorbidities are particularly susceptible to these severe clinical manifestations with coronavirus disease 2019 (COVID-19).MMP-9 is a matrix-degrading enzyme implicated in many biological processes, including inflammation; MMP-9 has been reported to activate latent transforming growth factor (TGF)-β to its active form and to induce TGF-β production in epithelial cells. TGF-β1 is believed to be a critical mediator of pathologic, fibrotic, and remodeling responses in the lung and other organs, and these responses are believed to be mediated by the ability of TGF-β1 to stimulate fibrogenic and apoptotic “injury” pathways, these observations have led to the suggestion that MMP-9 plays an important role in the tissue remodeling that characterizes many lung diseases. Indeed, TGF-β1 plays a central role in the pathogenesis of pulmonary fibrosis by promoting differentiation of fibroblasts into myofibroblasts that produce excessive extracellular matrix resulting in deteriorating lung function. Further, TGF-β is involved in the fluid homeostasis in the lung as well. Besides, numerous studies on the role of TGF–β in fibrosis models and various models of diseases including inflammatory and immune diseases have demonstrated the beneficial effect of blocking TGF–β.
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