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Project

Endothelial dysfunction in post-infection fatigue syndromes

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The mechanisms of the development of endothelial dysfunction, which has been described as one of the key factors for the symptoms of ME/CFS and Long Covid patients, are currently still largely unexplored. The project therefore aims to investigate key biological aspects related to endothelial cell function using plasma samples from an Austrian cohort of ME/CFS and Long Covid patients.

Post-infection chronic fatigue syndromes, such as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and post-COVID-19 condition (Long Covid), are conditions primarily characterized by debilitating fatigue. This fatigue can range from mild, where patients are still able to participate in some social activities (e.g., school, work), to moderate and severe, where sufferers are predominantly homebound and bedridden.

As a result, ME/CFS and Long Covid not only negatively impact the quality of life of affected individuals and their caregivers but also represent a substantial and often silent burden on healthcare systems worldwide, including Austria. This is primarily because most cases remain undiagnosed due to the lack of standardized clinical assessments and diagnostic markers.

Endothelial dysfunction, which is well known to affect blood flow, oxygen and nutrient delivery, and waste removal in the body, has been described as one of the key factors behind the symptoms experienced by ME/CFS and Long Covid patients. However, the mechanisms that might explain the development of endothelial dysfunction remain largely unexplored.

Therefore, this project aims to evaluate key biological aspects related to the function of endothelial cells – a layer of cells lining blood vessels – using plasma samples from an Austrian cohort of ME/CFS and Long Covid patients. We expect that the findings from our study will provide new insights to better understand endothelial dysfunction in post-infection chronic fatigue syndromes, leading to improved patient stratification and tailored treatment alternatives.

References:

1. Pipper C, Bliem L, León LE, Mennickent D, Bodner C, Guzmán-Gutiérrez E, Stingl M, Untersmayr E, Wagner B, Bertinat R, Sepúlveda N, Westermeier F (*). Sex and disease severity-based analysis of steroid hormones in ME/CFS. Journal of Endocrinological Investigation. 2024. doi: 10.1007/s40618-024-02334-1.

2. Bertinat R, Villalobos-Labra R, Hofmann L, Blauensteiner J, Sepúlveda N, Westermeier F (*). Decreased NO production in endothelial cells exposed to plasma from ME/CFS patients. Vascular Pharmacology. 2022. doi: 10.1016/j.vph.2022.106953.

3. Blauensteiner J, Bertinat R, León LE, Riederer M, Sepúlveda N, Westermeier F (*). Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients. Scientific Reports. 2021. doi: 10.1038/s41598-021-89834-9.

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