nerd
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So far, reduced Vascular Endothelial Growth Factor (VEGF) has been reported in ME but not consistently [1, 2]. Viral activity is one etiopathogenic theory for ME, including the one of SARS-CoV-2, also called Long-Covid or Post-Covid. Endothelial damage has been found in Post-Covid [3, 4]. Alpha-2 adrenergic agonism is a key regulator of endothelial constriction and dilation, dependant on the type of blood vessel [5]. Endothelial damage can reduce the endothelial alpha-2 adrenergic potential.
Based on the findings from Post-Covid, let's make the assumption that endothelial damage (post-acute or by residual viral activity) is a key driver of endothelial dysfunction as it is reasoned by some researchers. Wirth and Scheibenbogen focus a lot on the serology, metabolic, and cellular mechanisms of endothelial dysfunction. But I wonder if it might simply be a structural problem from viral activity in the endothelium or connective tissue or from the incapacity to rebuild it. The incapacity to rebuild it might manifest a trap situation in that the downstream effects from a dysfunctional endothelium are damaging the endothelium.
I know that infrared therapy and (near infra-) red therapy have already been discussed independently. But there are also two other methods that might be able to get deeper into the tissue. One is Intense Pulsed Light (IPL) therapy, the other is Photobiomodulation (PBM). PBM has shown to increase endothelial growth via VEGF [6, 7]. Infrared therapy, however, rather seems to induce autophagy, thereby protecting the endothelium from damage but also preventing endothelial growth [8, 9, 10]. If only we could with certainty say if there is residual viral activity or if there is no viral pathology present anymore and cell growth a safe choice.
Based on the findings from Post-Covid, let's make the assumption that endothelial damage (post-acute or by residual viral activity) is a key driver of endothelial dysfunction as it is reasoned by some researchers. Wirth and Scheibenbogen focus a lot on the serology, metabolic, and cellular mechanisms of endothelial dysfunction. But I wonder if it might simply be a structural problem from viral activity in the endothelium or connective tissue or from the incapacity to rebuild it. The incapacity to rebuild it might manifest a trap situation in that the downstream effects from a dysfunctional endothelium are damaging the endothelium.
I know that infrared therapy and (near infra-) red therapy have already been discussed independently. But there are also two other methods that might be able to get deeper into the tissue. One is Intense Pulsed Light (IPL) therapy, the other is Photobiomodulation (PBM). PBM has shown to increase endothelial growth via VEGF [6, 7]. Infrared therapy, however, rather seems to induce autophagy, thereby protecting the endothelium from damage but also preventing endothelial growth [8, 9, 10]. If only we could with certainty say if there is residual viral activity or if there is no viral pathology present anymore and cell growth a safe choice.
- Reductions in circulating levels of IL-16, IL-7 and VEGF-A in myalgic encephalomyelitis/chronic fatigue syndrome (2016) [0.1016/j.cyto.2015.11.018]
- Cytokine profiling of extracellular vesicles isolated from plasma in myalgic encephalomyelitis/chronic fatigue syndrome: a pilot study (2020) [10.1186/s12967-020-02560-0]
- Persistent endotheliopathy in the pathogenesis of long COVID syndrome (2021) [10.1111/jth.15490]
- Update on endothelial dysfunction in COVID-19: severe disease, long COVID-19 and pediatric characteristics (2021) [10.1515/labmed-2021-0134].
- Vasoconstrictive versus Vasodilatory Effects of Alpha-2 Adrenergic Agonists on the Spinal Microcirculation (2000) [10.1097/00000542-200005000-00043]
- Low level laser therapy increases angiogenesis in a model of ischemic skin flap in rats mediated by VEGF, HIF-1α and MMP-2 (2013) [10.1016/j.jphotobiol.2013.06.004]
- Phototherapy with low-level laser influences the proliferation of endothelial cells and vascular endothelial growth factor and transforming growth factor-beta secretion (2013) [pmid: 23959736]
- Far-infrared protects vascular endothelial cells from advanced glycation end products-induced injury via PLZF-mediated autophagy in diabetic mice (2017) [10.1038/srep40442]
- Far-infrared therapy induces the nuclear translocation of PLZF which inhibits VEGF-induced proliferation in human umbilical vein endothelial cells (2012) [10.1371/journal.pone.0030674]
- Far infrared therapy inhibits vascular endothelial inflammation via the induction of heme oxygenase-1 (2008) [10.1161/ATVBAHA.107.160085]