COVID-19-The Shift of Homeostasis into Oncopathology or Chronic Fibrosis in Terms of Female Reproductive System Involvement.
Elena V PetersenDaria A ChudakovaDaiana ErdyneevaDulamsuren ZorigtEvgeniya ShabalinaDenis GudkovPavel A KaralkinIgor ReshetovOspan A MynbaevPublished in: International journal of molecular sciences (2023)
The COVID-19 pandemic caused by the SARS-CoV-2 coronavirus remains a global public health concern due to the systemic nature of the infection and its long-term consequences, many of which remain to be elucidated. SARS-CoV-2 targets endothelial cells and blood vessels, altering the tissue microenvironment, its secretion, immune-cell subpopulations, the extracellular matrix, and the molecular composition and mechanical properties. The female reproductive system has high regenerative potential, but can accumulate damage, including due to SARS-CoV-2. COVID-19 is profibrotic and can change the tissue microenvironment toward an oncogenic niche. This makes COVID-19 and its consequences one of the potential regulators of a homeostasis shift toward oncopathology and fibrosis in the tissues of the female reproductive system. We are looking at SARS-CoV-2-induced changes at all levels in the female reproductive system.
Keyphrases
- sars cov
- extracellular matrix
- respiratory syndrome coronavirus
- public health
- stem cells
- endothelial cells
- mesenchymal stem cells
- high glucose
- transcription factor
- gene expression
- coronavirus disease
- oxidative stress
- drug induced
- human health
- liver fibrosis
- diabetic rats
- risk assessment
- vascular endothelial growth factor