RESUMO
SARS-CoV-2 infection is a significant health concern that needs to be addressed not only during the initial phase of infection but also after hospitalization. This is the consequence of the various pathologies associated with long COVID-19, which are still being studied and researched. Lung fibrosis is an important complication after COVID-19, found in up to 71% of patients after discharge. Our research is based on scientific articles indexed in PubMed; in the selection process, we used the following keywords: "lung fibrosis", "fibrosis mediators", "fibrosis predictors", "COVID-19", "SARS-CoV-2 infection", and "long COVID-19". In this narrative review, we aimed to discuss the current understanding of the mechanisms of initiation and progression of post-COVID-19 lung fibrosis (PC-19-LF) and the risk factors for its occurrence. The pathogenesis of pulmonary fibrosis involves various mediators such as TGF-ß, legumain, osteopontin, IL-4, IL-6, IL-13, IL-17, TNF-α, Gal-1, Gal-3, PDGF, and FGFR-1. The key cellular effectors involved in COVID-19 lung fibrosis are macrophages, epithelial alveolar cells, neutrophils, and fibroblasts. The main fibrosis pathways in SARS-CoV-2 infection include hypoxemia-induced fibrosis, macrophage-induced fibrosis, and viral-fibroblast interaction-induced fibrosis.
RESUMO
Inguinal hernia repair is one of the most commonly performed surgical activities worldwide. Given the circumstances, understanding and identifying the risk and the protective factors is an essential step in order to prevent, diagnose and treat such a common condition. For a long time, obesity was generally considered to be a risk factor in the occurrence of an inguinal hernia. Studies have provided some unexpected data, suggesting that it might actually be a protective factor. This review aims to provide an overview on this topic, taking into account systemic aspects such as collagen distribution and metabolism. In inguinal hernia patients, the ratio between type I collagen and type III collagen is decreased, with type III collagen being responsible for the weakness of the abdominal wall. In obese patients, the extracellular matrix becomes richer in collagen, especially type I collagen, which will generate strength and stiffness. Obesity seems to be a protective factor indeed, but in order to understand the underlying mechanism and to choose the optimal surgical approach, further research is needed.
