Leaky Vasculature, Leaky Gut, LEAKY (MISSING) CHANNELS: The Spike Protein and Connexin43

The Spike Protein significantly decreases the expression of Connexin43 (Cx43), a gap junction protein, implicated in Sudden Cardiac Death.

Immunofluorescent staining for Cx43 in wild-type and MHC-CKO hearts. Sections from E12.5 (A through C) and 4-week-old (D through F) hearts were stained for Cx43 (green fluorescent stain), counter-stained using wheat germ agglutinin (red fluorescent stain), and imaged with confocal microscopy. Abundant Cx43 staining in control littermate hearts is evident at both embryonic (A) and postnatal (D) stages. In contrast, extensive areas of the myocardium in embryonic (B and C) and postnatal (E and F) CKO mice are devoid of Cx43 staining, although some residual expression is detectable. Bar=50 μm. 

Spike Protein induced myocarditis is certainly a cause of the emerging sudden cardiac deaths being observed, particularly in the young. However, a great number of the young perishing from sudden cardiac death do not seem to have suffered myocarditis. I am certain other Spike Protein mechanisms are at work, and I have discussed some. I have now found what I consider to be a major factor in the surge of sudden cardiac deaths. That is the eradication of Cx43, a gap junction protein, by the Spike Protein. They are intimately related to ventricular arrhythmias. 

Gap junction channels, composed of highly homologous proteins known as connexins in vertebrate species, have been implicated in diverse processes, including the electrotonic coupling of excitable tissues, such as cardiac muscle. Theoretical modeling and studies of connexin (Cx) expression in diseased human and experimental animal hearts suggest that altered gap junction expression or function may underlie the high incidence of arrhythmias associated with many forms of heart disease, including hypertrophic, ischemic, and dilated cardiomyopathies. Specifically, in diseased myocardium, Cx43, the major constituent of ventricular gap junctions, is often diminished in abundance and fails to preferentially localize to the intercalated disk. This pathologic process, referred to as gap junction remodeling, is hypothesized to be an essential component of the substrate promoting some atrial as well as lethal ventricular tachyarrhythmias. 

Conduction Slowing and Sudden Arrhythmic Death in Mice With Cardiac-Restricted Inactivation of Connexin43 
https://www.ahajournals.org/doi/10.1161/01.RES.88.3.333 

We know that the presence of Spike Protein significantly diminishes the expression of this protein. 

The expression of VE-Cadherin, an endothelial adherens junction protein, JAM-A, a tight junctional protein, Connexin-43, a gap junctional protein, and PECAM-1, were all decreased significantly after Spike treatment in control and to a greater extent, in diabetic cells.

SARS-CoV-2 Spike Protein Induces Degradation of Junctional Proteins That Maintain Endothelial Barrier Integrity 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8225996/ 

Once we examine the results of Cx43 loss, we begin to see a picture clearly emerge. Indeed, this protein’s dysregulation is found in SIDS (Sudden Infant Death Syndrome) as well as instances of sudden cardiac death. 

This is the first study to implicate a mutation in a connexin protein in the pathogenesis of SIDS. E42K-Cx43 demonstrated a severe loss-of-function phenotype and is located in a crucial conserved region of the protein. Although such SIDS-associated Cx43 mutations are rare, this study provides evidence for the contribution of Cx43 dysregulation to sudden death and contributes to the growing body of literature implicating cardiac arrhythmias as the cause of a subset of deaths caused by SIDS. 

Connexin43 Mutation Causes Heterogeneous Gap Junction Loss and Sudden Infant Death 
https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.111.057224 

In conclusion, the expression of myocardial Cx43 significantly decreased in sudden death patients with hyperthyroid heart disease. Our findings suggest that decreased expression of Cx43 may be related to sudden death of hyperthyroid heart disease. 

Disturbed expression and distribution of myocardial connexin 43 in sudden death patients with hyperthyroid heart disease 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6965932/ 

After the recent findings that SARS-CoV-2 and the Spike Protein disrupt tight junctions virtually everywhere, I decided to look into the gap junctions. Clearly, this is a major leitmotiv of Spike Protien pathology. I will continue to investigate. 

Thank you for your continued support, readership and dialog. This one was worth burning the midnight oil.