ABSTRACT
The vascular niche is a microenvironment located around capillaries and is mainly composed of endothelial cells, pericytes, macrophages, lymphocytes, mesenchymal stem cells, and hematopoietic stem cells. Studies have found that the vascular niche not only functions to regulate cell growth and differentiation in normal tissues, but also has an important role in regulating fibrosis in various organs and tissues in disease states. Coronavirus disease 2019 (COVID-19) is a systemic disease that broke out in 2019, caused by SARS-CoV-2 infection, which results in pulmonary inflammation, systemic multi-organ damage, and an inflammatory cytokine storm. Recently, the vascular niche has been found to play a role in COVID-19-related multi-organ damage. In this review, we introduce the important role of the vascular niche in organ fibrosis and COVID-19-related organ damage, summarize some of the cellular signaling pathways in the vascular niche that promote fibrosis, and discuss the treatment of organ fibrosis in Traditional Chinese medicine and Western medicine.
ABSTRACT
INTRODUCTION: The coronavirus disease 2019 (COVID-19), emerged in late 2019, was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The risk factors for idiopathic pulmonary fibrosis (IPF) and COVID-19 are reported to be common. This study aimed to determine the potential role of differentially expressed genes (DEGs) common in IPF and COVID-19. MATERIALS AND METHODS: Based on GEO database, we obtained DEGs from one SARS-CoV-2 dataset and five IPF datasets. A series of enrichment analysis were performed to identify the function of upregulated and downregulated DEGs, respectively. Two plugins in Cytoscape, Cytohubba and MCODE, were utilized to identify hub genes after a protein-protein interaction (PPI) network. Finally, candidate drugs were predicted to target the upregulated DEGs. RESULTS: A total of 188 DEGs were found between COVID-19 and IPF, out of which 117 were upregulated and 71 were downregulated. The upregulated DEGs were involved in cytokine function, while downregulated DEGs were associated with extracellular matrix disassembly. Twenty-two hub genes were upregulated in COVID-19 and IPF, for which 155 candidate drugs were predicted (adj.P.value < 0.01). CONCLUSION: Identifying the hub genes aberrantly regulated in both COVID-19 and IPF may enable development of molecules, encoded by those genes, as therapeutic targets for preventing IPF progression and SARS-CoV-2 infections.