Pulmonary fibrosis in COVID-19: mechanisms, consequences and targets
Steven O’Reilly
Abstract
Pulmonary fibrosis is characterized by extracellular deposition in the lung primarily collagen but also other ECM molecules. The primary cell type responsible for this is the myofibroblast, and this can be induced by various stressors and signals. Infections be they bacterial or viral can cause pulmonary fibrosis (PF). In 2019, severe acute respiratory syndrome coronavirus 2 (SAR-CoV-2) originated in Wuhan, China, has led to a worldwide pandemic and can lead to acute respiratory distress and lung fibrosis. The virus itself can be cleared, but patients may develop long-term PF, which can be debilitating and life-limiting. There is a significantly perturbed immune response that shapes the fibrotic response leading to fibrosis. Given the importance of PF irrespective of cause, understanding the similarities and differences in pathogenesis caused by SARS-CoV-2-induced PF may yield new therapeutic targets. This review examines the pathology associated with the disease and discusses possible targets.