What is it about?
In this study, we investigated how the virus that causes COVID-19 can enter vascular endothelial cells through mechanisms that do not rely on the ACE2 receptor, a process that may contribute to the development of severe disease. We discovered that aged, or senescent, endothelial cells have an increased ability to take up the virus and respond with heightened inflammation.
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Why is it important?
Almost six years after its emergence, COVID-19 continues to cause more severe illness and deaths than other respiratory infections. While vascular damage is a hallmark of severe cases, how the virus enters blood vessel cells was unclear. Our study shows that senescent endothelial cells—aged and dysfunctional cells—take up the virus through an ACE2-independent pathway and trigger strong inflammation. This highlights cellular aging as a key factor in disease severity and points to new approaches for protecting older adults.
Perspectives
These findings point to the potential of developing new preventive and therapeutic strategies for severe COVID-19 by targeting senescent endothelial cells, particularly in elderly individuals who are at higher risk.
Kyoko Hida
Hokkaido University
Read the Original
This page is a summary of: SARS-CoV-2 uptake and inflammatory response in senescent endothelial cells are regulated by the BSG/VEGFR2 pathway, Proceedings of the National Academy of Sciences, July 2025, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2502724122.
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