Impaired microcirculation and tissue hypoxia as a possible mechanism in ME/CFS

Project description

There is increasing evidence that the blood supply to tissues in ME/CFS patients is poorly regulated. Based on published and preliminary data, the investigators hypothesise that tissue hypoxia due to impaired microcirculation is a key element that disrupts cellular energy metabolism in patients.

To address this, the project team will analyse extracellular adenosine triphosphate (ATP) and other biochemical signatures of hypoxia in the blood of ME/CFS and Long COVID patients collected at rest and during exercise testing. They will also investigate changes in circulating endothelial microparticles, erythrocytes, and neutrophils, as possible novel mediators of the pathomechanism. The team will pursue the mechanisms involved through hypothesis-driven approaches in patient samples and laboratory studies, using beyond state-of-the-art approaches. They will test the following hypotheses:

1) Impaired microcirculation and tissue hypoxia play a role in ME/CFS, in an exertion-dependent manner;

2) Endothelial dysfunction and erythrocyte alterations contribute to impaired microcirculation in ME/CFS; and

3) Altered neutrophil activity is associated with impaired microcirculation in ME/CFS.

The results will provide new insights into the mechanism of ME/CFS and Long COVID, identify new avenues for future research, and uncover possible opportunities for clinical translation. The project will involve collaboration with leading scientists with complementary expertise and resources in the field.

Description adapted from project website: see link above.