Why spike protein containing or mRNA transcription to self-produce the spike protein (S-protein) is likely to increase blood clotting and inflammation, especially in at-risk individuals:
The SARS-CoV2 (SARS2) spike protein is biologically active.
ahajournals.org/doi/full/10.11…
The injected S protein (or program via mRNA to induce self-production of the S protein) alone damages vascular endothelial cells (ECs) in vitro and in vivo, manifested by impaired mitochondrial function, decreased ACE2 expression and eNOS activity, and increased glycolysis.
Increased glycolysis indicates impairment of the mitochondria. Upregulation of this pathway activates inflammatory signalling cascades. The decrease in eNOS activity further increases vasoconstriction.
ahajournals.org/doi/full/10.11…
Normally healthy people will fight communicable infection exposure at the mucosal level, in the nasal pharyngeal region. Less health people further into the lungs. Very unhealthy people, it gets into the vascular system.
Injecting substances containing the spike protein or that gets your own cells to manufacture the spike protein, means bypassing all these levels.
Angiotensin II (AngII) increases blood pressure & inflammatory pathway signalling, reduces nitric oxide production, increases extracellular matrix degradation, increases fibrous growth etc.
ACE2 receptors, enzymatically convert AngII to angiotensin (1-7) (Ang(1-7)).
The S-protein is biologically active
portlandpress.com/clinsci/articl…
The action of stimulating ACE2, also sends in an intracellular signal into the cell, as a method of telling the cell "what is going on outside of itself".
The cell receives this information about higher blood pressure. The cell then responds to that dynamic. eg, increasing inflammatory actions, when ACE2 is stimulated, it increases the action of NADPH-oxidase, this basically means inflammation activation.
The product of AngII converted into Ang(1-7) is important, as Ang(1-7) is the counter regulation to AngII (the one that increases blood pressure).
Ang(1-7) reacts with another receptor called MasR, which dials down/modulates the inflammatory signalling and...
....enables the production of nitric oxide, to help relax the micro-vasculature, to prevent clotting.
So, where does the S-protein come into this?
It activates the ACE2 receptor, like AngII, but there is no conversion product to Ang(1-7),...
....instead, it is somewhat akin to having an increase in AngII. If the S-protein is complete, it also will induce receptor endocytosis (the taking in of the receptor into the cells), which means, existing AngII in the system, stays around even longer,....
...inducing more actions that increase inflammation, clotting & blood pressure dysregulation, whilst decreases converted counter regulatory product of Ang(1-7) that works as a feedback mechanism, eg to decrease NADPH-oxidase (which increases reactive oxygen species formation).
In a relatively healthy person, they can "get away with it".
Eg, I am in ketosis. You could inject me with some insulin so my blood glucose goes down to 3mmol/L, and I am unlikely to suffer a hypoglycaemic coma, as I have a good buffering capacity (my brain is well adapted to..
..using ketones, so won’t stress from temporary decrease in glucose). This will be similar with regards to a temporary increase in AngII or the S-protein from either wild corona virus or vaccine introduced (either via modified adenovirus form or mRNA induced endogenous synthesis)
It will mess with homeostatic regulation, and anyone who is already dysregulated, will have a tougher time with this.
The people who are having really serious negative responses, have a degree of compromised health that is not obvious, not picked up, undiagnosed.
Hyperinsulinaemia exists in lean individuals, and occurs easily a decade before overt symptoms. This is why some seemingly younger healthy-ish individuals are having awful responses. Just like to the real deal wild virus, as they would likely to many communicable infections.
Only, those people (the healthy-ish and healthy) would normally only face these infections in their natural acquisition habitat, meaning for a respiratory infection, it would challenge them in the oral and nasal cavities, at the mucosal layer, and not make it into deep tissues.
Injecting into intramuscular bypasses these layers of natural barriers that fight infection first...
The full-length S1 subunit of SARS-CoV-2 alone, at a concentration as low as 130 pmol/L activates MEK the activator of extracellular signal-regulated kinase (ERK) part of the MAPK signal transduction pathway.
nature.com/articles/72901…
mdpi.com/2076-393X/9/1/…
It makes sense that activation of ACE2 receptor induces an intracellular signal transduction cascade, as this receptor spans the plasma membrane. Biologically, receptors that do transduce extracellular into intracellular signals, span membranes.
If they were not to induce an intracellular response, they would be plugged into the extracellular membrane and not all the way through to the other side. Biology 101, structure dictates function.
Furthermore, with regards to viral evolution, viruses "found" a way to gain entry into our cells while simultaneously activating cell "building/making programs", so that the virus gets replicated. In the case of SARS2 it is via the ACE2 receptor...
Activation then causes intracellular activation of the MAPK pathway, which is the growth and division pathway. This makes sense in terms of viruses taking advantage of cell signalling dynamics as the virus "wants" to get the cell to increase making of stuff, including themselves,
and then dividing. Of course, the virus has no sentient intentions, this is just something that they have evolved to cash in on...
In most people who are not severely hyperinsulinaemic nor have other diseases that compromise the whole system, most people will fight a respiratory infection in their nose and throat, and then the lungs at the mucosal level, where the virus either never gains systemic entry,...
or very little entry to cause mass scale harm.
Intra-muscular injection, containing S-protein or S-protein synthesis inducing mRNA, by-passes this barrier. Those who are unaware that they have chronic pernicious hyperinsulinaemia, are more likely to be adversely affected
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