'Abnormal Fibrous Clotting' - The Science Is Coalescing Almost As Fast As The Clots Themselves

Following my post yesterday, I came across this post today:

"CD147 contributes to SARS-CoV-2-induced pulmonary fibrosis"

I would have liked to have commented but once again, only paid subscribers can comment. I have to say, I’m increasingly finding that Substack is not conducive to open discussion. Too many authors are limiting replies to their posts by using a paywall. So, I’ll say in more detail what I would have liked to have said on Jessica’s post. Don’t get me wrong; I’m certainly no expert and have no training whatsoever in this stuff, which I find incredibly complex and difficult to understand, but I am rather good at detecting common themes and patterns emerging from fearfully complex subjects.

Jessica says:

Please refer to my previous article entitled: “Is SARS-nCoV-2-associated systemic micro-clotting due to spike protein-induced hemolysis resulting in amyloid plaque formation?”.

Then refer to a new publication entitled: “CD147 contributes to SARS-CoV-2-induced pulmonary fibrosis” published on November 25, 2022 in Nature Signal Transduction and Targeted Therapy. This is a published article which means it’s been peer-reviewed.

So I did.

Pulmonary fibrosis is basically life threatening out of control scarring (fibrosis) of the lungs in response to injury, in this case injury due to severe Covid-19. Jessica describes it thus:

As most of you know by now, in severe cases of COVID-19, for reasons as yet to be meticulously defined, severe lung pathologies can develop including pulmonary fibrosis. Pulmonary (lung) fibrosis (development of connective tissue as a repair function due to injury - which is normal) is very serious for the same reason myocardial scarring (or any pathological tissue scarring for that matter) is very serious. Inevitably, prevention of normal functioning of the tissue/organ - due to the replacement of normal cells or tissues with scar tissue - ensues.

Imagine if you replaced the rubbery surface of a balloon with sections or grafts of inflexible cardboard and then tried to blow up the balloon. It would pop because the paper is not flexible. Connective tissue formation is absolutely normal - essential, in fact - to our normal functioning. I mean, what would we do if we didn’t have connective tissue? We would simply fall apart! Like the narrative is doing!

In all complex systems, problems arise when normal functions go straight up pathological. In the case of pulmonary fibrosis, unregulated production of connective tissue in the lungs due to extended inflammatory reactions leads to lung malfunction and death.

CD147 (like ACE2) is a receptor found on human cells which binds to the spike region of the virus, allowing the virus to enter and infect the cell. It’s now recognised that CD147 is even more important in cell binding than ACE2. But it does something more:

Here, we identified a novel function of CD147 contributing to fibroblasts activation in COVID-19 pulmonary fibrosis besides mediating entry of virus and inducing cytokine storm.

Apart from many elevated cytokines and chemokines exerting profibrotic functions in fibrogenesis (IL-4, IL-6, IL-17, IFN-γ, CCL2, CCL4, IL-10, CXCL9, CXCL10, etc.), the main profibrogenic cytokine TGF-β and activation of TGF-β pathway were found to increase in lungs of SARS-CoV-2-infected hCD147 mouse model (Fig. 2b, c). During the initiation of the pulmonary fibrotic phase, epithelial cell injury and the activation of inflammation promote the production of TGF-β, which plays a critical role in the process by which fibroblasts differentiate into myofibroblasts, produce collagen, reduce lung elasticity and impair respiratory function2

Jessica explains it rather more clearly:

So what’s new here is that in addition to the established functions of CD147 as a receptor for cell entry/infection and also cytokine storm mediators, they actually act as critical regulators of fibroblast activation in the SARS-CoV-2 context. The implications are quite staggering since they propose that a positive feedback loop - that has been identified in liver fibrosis and hepatocellular carcinoma - may also play a role in the context of lung fibrosis mediated by fibroblast activation.910 This positive feedback loop involves none other than TGF-β (and CD147), of course. You can read a little more about TGF-β here and here and here (if you like Wikipedia).11

So this is crucial. The activation of CD147 by binding to the spike protein of the virus initiates a positive feedback loop involving the TGF-β pathway, where an initial inflammation of endothelial cells and resulting fibrosis results in the stimulation of yet more fibrosis. Sound familiar? Those long, stringy, fibrous clots found in corpses which have grown so large they actually completely obstruct the veins and arteries in which they are growing? This is a catastrophic health outcome, the equivalent of a fast growing fibrous cancer inside the circulatory system of human beings.

I found another science paper which might explain this positive feedback loop. It was published in 2010, meaning that at least a decade prior to the mass rollout of the spike-based Covid ‘vaccines’ it was known by medical scientists that blood fibrinogen triggers the TGF-β pathway.

Here we show that the blood protein fibrinogen, which leaks into the CNS immediately after blood–brain barrier (BBB) disruption or vascular damage, serves as an early signal for the induction of glial scar formation via the TGF-β/Smad signaling pathway.

Inhibition of the TGF-β receptor pathway abolishes the fibrinogen-induced effects on glial scar formation in vivo and in vitro. These results identify fibrinogen as a primary astrocyte activation signal, provide evidence that deposition of inhibitory proteoglycans is induced by a blood protein that leaks in the CNS after vasculature rupture, and point to TGF-β as a molecular link between vascular permeability and scar formation.

According to what Jessica is saying, this triggering of the TGF-β itself stimulates the production of more fibrosis and so it continues, a vicious circle resulting in runaway scar tissue formation or fibrous clot formation inside veins and arteries for as long as the spike protein remains present and continues binding to CD147.

The authors refer to TGF-β as the master regulator of organ fibrosis. Nice. So what this means is that there’s a system of fiber formation that once initiated, keeps itself going. Not good for lungs.

Again, I go back to 13 months ago and quote from my own analysis of a recently released study. I said at the time and quoted directly from the study:

“It's not just spike proteins building abnormal blood clots which is a problem though, it's even worse. The spike-induced fibrin accumulation at bodily sites actually causes more inflammation:”

Fibrin is deposited locally at sites of vascular damage and is a potent proinflammatory activator and a key inducer of oxidative stress (11, 18). Strikingly, Spike increased fibrin-induced release of reactive oxygen species (ROS) in a concentration-dependent manner in bone marrow derived macrophages (BMDMs), while Spike alone did not have an effect (Fig. 1G). These results suggest a role for Spike as an enhancer of fibrin-induced inflammation at sites of vascular damage. Overall, these results reveal an unanticipated role for SARS-CoV-2 Spike as a fibrinogen binding protein that alone accelerates the formation of abnormal clots with altered structure and increased inflammatory activity.

Another quote from the actual study:

Our findings now show that coagulopathy is not merely a consequence of inflammation. Rather, the interaction of SARS-CoV-2 Spike with fibrinogen and fibrin results in abnormal blood clot formation that in turn drives inflammation.

So there’s your pro-inflammatory positive feedback loop explained in a scientific study published in October 2021 and there is your direct link between pulmonary fibrosis, huge white rubbery ‘blood’ clots and the presence of SARS-CoV-2 genetically engineered and patented spike protein, either by infection with SC-2 virus or by injection with the Covid gene-based ‘vaccines’. The fact that the white rubbery blood clots were not being observed prior to the mass vaccination campaign suggests very strongly that the spike activation of CD147 and the triggering of the TGF-β pathway is much more dangerous in vaccinated people who have trillions of these spikes in their blood stream and organs, which have been modified to be more resistant to degradation than the viral spike.

Governments are still pushing this crap into people’s arms. So are health authorities and many other institutions. When are they all going to be prosecuted and thrown into prison to rot for being complicit in an iatrogenocide?