An Examination of the Mechanism

Whether induced surgically or by hypertension, infections, extreme heat, or caustic chemicals, tissue injury invariably leads to vasodilatation, with subsequent leakage of plasma proteins into the connective tissues, rapid activation of the coagulation cascade, and deposition of fibrin. A central paradigm in the field is that the fibrin is organized into a “provisional fibrin matrix,” which acts as a road map to direct the migration of invading cells. Leukocytes and possibly fibroblasts migrate into the area and elaborate cytokines which, in turn, stimulate resident cells to synthesize and deposit collagens and other insoluble fibrillar components into the evolving extracellular matrix (ECM).

Fibrotic disease occurs when normal control of this process is compromised and excess fibrous material accumulates in the tissues. It is generally assumed that the persistence of fibrin in the matrix promotes fibrosis, and that the extent of fibrosis is limited by proteinases that remove the fibrin (i.e., the fibrinolytic system). In a recent issue of the JCI, Hattori et al. (1) affirm previous suggestions that plasminogen activator inhibitor-1 (PAI-1) promotes pathological fibrosis but challenges the concept that fibrin is required.

The Spike Protein is a “Turnkey Solution” to induce this coagulation and fibrotic cascade. It SIMULTANEOUSLY creates the effect of vasodilation by inducing degradation of junctional proteins that maintain endothelial barrier integrity, allowing for the rapid activation of the coagulation cascade, and deposition of fibrin. A study showed that Spike alone was able to induce disruption of endothelial barrier integrity in control cells. Expectedly, these results also show that diabetic endothelial barrier permeability is affected in untreated cells and that Spike induced an even greater disruption of endothelial barrier function. THIS EXPLAINS WHY DIABETICS ARE MORE AT RISK.

In addition, the Spike Protein generates AMPLE PAI-1, which ALONE AND WITHOUT FIBRIN can induce Coagulation and Fibrosis! It was shown that the rSARS-CoV-2-S1 (recombinant severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2] viral envelope spike) glycoprotein stimulated ROBUST PRODUCTION of PAI-1 by human pulmonary microvascular endothelial cells (HPMECs).

Without question, the current approach must be paused while this is investigated. I am certain it will be proven true.

Referenced/Related Papers

PAI-1, fibrosis, and the elusive provisional fibrin matrix

ZMPSTE24 Regulates SARS-CoV-2 Spike Protein–enhanced Expression of Endothelial PAI-1

SARS-CoV-2 Spike Protein Induces Degradation of Junctional Proteins That Maintain Endothelial Barrier Integrity