<p>The COVID-19 pandemic has resulted in several long-term complications, with COVID-19-induced pulmonary fibrosis being a significant concern. Despite increasing recognition, the mechanisms underlying its development, effective treatment strategies, and long-term outcomes remain poorly understood. Emerging research highlights the direct impact of SARS-CoV-2 on vascular endothelial cells, identifying endothelial-mesenchymal transition (EndMT) as a key factor in the progression of COVID-19-induced pulmonary fibrosis. However, there is a notable lack of comprehensive reviews addressing the link between EndMT and COVID-19-induced pulmonary fibrosis. This review seeks to fill that gap by providing an in-depth analysis of the relationship between EndMT and fibrosis, examining relevant risk factors and molecular pathways. Our findings offer critical insights that could inform the development of targeted anti-fibrotic therapies aimed at mitigating COVID-19-related pulmonary fibrosis. Ultimately, this review aims to advance understanding of the role of EndMT in pulmonary fibrosis and to guide future research and treatment approaches.</p>

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Unveiling the secret of cellular metamorphosis: the crucial role of EndMT mechanisms in COVID-19-induced pulmonary fibrosis

  • Xin Zhang,
  • Xia Tong,
  • Ruijie Hou,
  • Pengbo Wang,
  • Yan Mo,
  • Lanlan Zhang

摘要

The COVID-19 pandemic has resulted in several long-term complications, with COVID-19-induced pulmonary fibrosis being a significant concern. Despite increasing recognition, the mechanisms underlying its development, effective treatment strategies, and long-term outcomes remain poorly understood. Emerging research highlights the direct impact of SARS-CoV-2 on vascular endothelial cells, identifying endothelial-mesenchymal transition (EndMT) as a key factor in the progression of COVID-19-induced pulmonary fibrosis. However, there is a notable lack of comprehensive reviews addressing the link between EndMT and COVID-19-induced pulmonary fibrosis. This review seeks to fill that gap by providing an in-depth analysis of the relationship between EndMT and fibrosis, examining relevant risk factors and molecular pathways. Our findings offer critical insights that could inform the development of targeted anti-fibrotic therapies aimed at mitigating COVID-19-related pulmonary fibrosis. Ultimately, this review aims to advance understanding of the role of EndMT in pulmonary fibrosis and to guide future research and treatment approaches.