A team of researchers, including Associate Prof Rob Wüst who is currently working on a project funded by ME Research UK, have reviewed the evidence relating to biological aging (senescence) – which leads to a gradual deterioration in functioning – of endothelial cells as a potential disease mechanism of ME/CFS, and of long COVID.
Endothelial cells line both the inner surface of blood vessels, and the tube-like structures which transport a lymph – a fluid containing infection-fighting white blood cells – around the body.
Cells enter a state of senescence following persistent and unresolved stress, this can happen due to oxidative stress or tumour formation, or – more recently discovered – through viral infection. According to the research team:
“Virus-induced endothelial senescence, potentially in genetically susceptible individuals, has the potential to explain the symptoms and chronicity of ME/CFS and Long COVID, and hence warrants further investigation”
In their paper, the researchers say that senescence of endothelial cells can lead to:
- Abnormalities with blood flow, and in the process in which blood vessels narrow (vasoconstriction),
- Immune dysfunction,
- Impaired tissue repair,
- Increased oxidative stress levels,
- Blood clotting abnormalities.
Although more research is needed, the article published in the nature journal ‘Cell Death & Disease’, concluded that:
“The recognition of endothelial cell dysfunction and senescence as a core element in the aetiology of both ME/CFS and Long COVID should aid in the establishment of effective biomarkers and treatment regimens.”
