Microvascular Dysfunction and Basal Membrane Thickening in Skeletal Muscle in ME/CFS and Post-COVID, 2025, Slaghekke et al

[SNT Gatchaman]

From the Amsterdam PAIS 2026 conference thread —

Topics included muscle and blood-vessel abnormalities, post-exertional malaise (PEM), cellular waste, gene regulation, fat metabolism, and changes in brain tissue.

Another member of Rob’s team, PhD student Anouk Slaghekke, spoke about ME Research UK – funded research which had identified endothelial dysfunction specifically relating to the capillaries within muscle tissue of people with ME/CFS, and those with long COVID. Interestingly, Anouk’s findings suggest that it may not only mean that it is harder for oxygen to reach muscles in people with ME/CFS and in those with long COVID, but that it may be harder for waste products to leave muscle cells.

Interestingly, this last point was a central theme of Jelle Huijts’ presentation which indicated that there may be cellular waste build up in the skeletal muscle of people with ME/CFS. Jelle specifically spoke about a cellular waste product called lipofuscin, often known as the “wear-and-tear” or “age” pigment as it progressively accumulates inside the cells of living organisms as they age. A build-up of lipofuscin is linked to problems with how cells work. Previous research, although not specifically in people with ME/CFS, has linked it to the incomplete breakdown of damaged mitochondria.

 

[Jonathan Edwards]

From the Amsterdam PAIS 2026 conference thread —

I am sceptical that those observations link up in the way implied. I doubt lipofuscin accumulation is due to a diffusion problem. I may be wrong but the whole field seems to be full of such simplistic suggested connections without much evidence of them having been thought through.

Denatured proteins are likely to be cleared via lymphatics rather than by back diffusion across venules and capillaries.