Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients, 2021, Blauensteiner et al

https://www.nature.com/articles/s41598-021-89834-9

ABSTRACT
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disease characterized by unexplained debilitating fatigue. Although the etiology is unknown, evidence supports immunological abnormalities, such as persistent inflammation and immune-cell activation, in a subset of patients. Since the interplay between inflammation and vascular alterations is well-established in other diseases, endothelial dysfunction has emerged as another player in ME/CFS pathogenesis. Endothelial nitric oxide synthase (eNOS) generates nitric oxide (NO) that maintains endothelial homeostasis. eNOS is activated by silent information regulator 1 (Sirt1), an anti-inflammatory protein. Despite its relevance, no study has addressed the Sirt1/eNOS axis in ME/CFS. The interest in circulating microRNAs (miRs) as potential biomarkers in ME/CFS has increased in recent years. Accordingly, we analyze a set of miRs reported to modulate the Sirt1/eNOS axis using plasma from ME/CFS patients.

Our results show that miR-21, miR-34a, miR-92a, miR-126, and miR-200c are jointly increased in ME/CFS patients compared to healthy controls. A similar finding was obtained when analyzing public miR data on peripheral blood mononuclear cells. Bioinformatics analysis shows that endothelial function-related signaling pathways are associated with these miRs, including oxidative stress and oxygen regulation. Interestingly, histone deacetylase 1, a protein responsible for epigenetic regulations, represented the most relevant node within the network. In conclusion, our study provides a basis to find endothelial dysfunction-related biomarkers and explore novel targets in ME/CFS.

 

Discussion from author here:
https://twitter.com/user/status/1394963176698126340


Lots of work/findings on endothelial cells / function recently, including in POTS. I have no idea what they are / do. :-$

 

From the paper, for info.

"Acknowledgements

This study was supported by ME Research UK (SCI charity number SC036942) and carried out using samples from the UK ME/CFS Biobank, which were processed and stored at the UCL-RFH BioBank). The authors thank all the study participants for donating their blood to the UK ME/CFS Biobank (UKMEB) and also the ME/CFS community who raised funds to facilitate the UKMEB projects. The authors also want to thank the ME/CFS Society Austria (Österreichische Gesellschaft für ME/CFS, CFS-Hilfe), and the FH JOANNEUM University of Applied Sciences for supporting gran applications. FW thanks Mr. Mika Remes (QIAGEN) for his technical assistance. Finally, FW especially thanks Mr. Luis Westermeier for his support and encouragement throughout this study."

 

Could this have anything to do with anti-ETAR antibodies? Or would that be totally irrelevant for this matter?

 

https://twitter.com/user/status/1395369853217873921

 

Histone deacetylase has come up a few times over the past decade.

1) In 2011, Lenny Jason found, in this paper

2) A group at Brussels has set up a study that that will look at HDAC genes under PEM.

https://clinicaltrials.gov/ct2/show/NCT04378634

3) One of the more interesing papers, imo, of recent years was Neil McGregor's "Hypermetabolism" findings, which included blood and urine testing and indicated, amongst other things, problems with purine metabolism.

 

I believe there might be use in going to see if it pinged any other epigentic me/cfs studies, but I'm too tired to do that atm.