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What is going on with the claims of fibrin (stringy clots) found in some bodies at autopsy in the last few years? If this is true, what is the cause? Does it have any connection to COVID-19, COVID-19 mRNA vaccines? A combination of both? Or what?
Please see some of our studies (there are more):
Geroscience . Liver alterations and detection of SARS-CoV-2 RNA and proteins in COVID-19 autopsies
Am J Clin Pathol . Postmortem Histopathologic Findings and SARS-CoV-2 Detection in Autopsy Kidneys of Patients With COVID-19: A Systematic Review and Meta-Analysis
Ups J Med Sci . COVID-19: Not a thrombotic disease but a thromboinflammatory disease
Diagn Pathol . Evidence of autoinflammation as a principal mechanism of myocardial injury in SARS-CoV-2 PCR-positive medical examiner cases
Intern Med . Role of Fibrin Monomer Complex in Coronavirus Disease 2019 for Venous Thromboembolism and the Prognosis
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Fibrin -
snip
"Fibrin Formation, Structure, and Stability
During coagulation, fibrinogen is converted into insoluble fibrin (Figure 1). Fibrin formation involves thrombin-mediated proteolytic cleavage and removal of N-terminal fibrinopeptides from the Aα and Bβ chains. Insertion of these newly exposed α- and β-knobs into a- and b-holes in the γC and βC regions of the D nodule, respectively, on another fibrin monomer permits the half-staggered association of fibrin monomers into protofibrils. Subsequent aggregation of protofibrils into fibers yields a fibrin meshwork that is essential for blood clot stability. This process has been extensively reviewed.7–11
Clot formation, structure, and stability are strongly influenced by the conditions present during fibrin generation. These include the concentrations of procoagulants, anticoagulants, fibrin(ogen)-binding proteins, molecules,12–20 and metal ions,21,22 as well as contributions of blood and vascular cells, cell-derived microvesicles,23–30 and presence of blood flow31,32 (Figure 2). Many of these mechanisms have been reviewed.33,34.."
source: https://www.ahajournals.org/doi/full...AHA.117.308564
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snip
"Fibrin formation, structure, and stability are regulated by various genetic, biochemical, and environmental factors, allowing for dynamic kinetics of fibrin formation and structure. Interactions between fibrinogen and/or fibrin and plasma proteins and receptors on platelets, leukocytes, endothelial cells, and other cells enable complex functions in hemostasis, thrombosis, pregnancy, inflammation, infection, cancer, and other pathologies. Disorders in fibrinogen concentration and/or function increase risk of bleeding, thrombosis, and infection."
source: https://onlinelibrary.wiley.com/doi/...002/rth2.12191
Please see some of our studies (there are more):
Geroscience . Liver alterations and detection of SARS-CoV-2 RNA and proteins in COVID-19 autopsies
Am J Clin Pathol . Postmortem Histopathologic Findings and SARS-CoV-2 Detection in Autopsy Kidneys of Patients With COVID-19: A Systematic Review and Meta-Analysis
Ups J Med Sci . COVID-19: Not a thrombotic disease but a thromboinflammatory disease
Diagn Pathol . Evidence of autoinflammation as a principal mechanism of myocardial injury in SARS-CoV-2 PCR-positive medical examiner cases
Intern Med . Role of Fibrin Monomer Complex in Coronavirus Disease 2019 for Venous Thromboembolism and the Prognosis
---------------------------------
Fibrin -
snip
"Fibrin Formation, Structure, and Stability
During coagulation, fibrinogen is converted into insoluble fibrin (Figure 1). Fibrin formation involves thrombin-mediated proteolytic cleavage and removal of N-terminal fibrinopeptides from the Aα and Bβ chains. Insertion of these newly exposed α- and β-knobs into a- and b-holes in the γC and βC regions of the D nodule, respectively, on another fibrin monomer permits the half-staggered association of fibrin monomers into protofibrils. Subsequent aggregation of protofibrils into fibers yields a fibrin meshwork that is essential for blood clot stability. This process has been extensively reviewed.7–11
Clot formation, structure, and stability are strongly influenced by the conditions present during fibrin generation. These include the concentrations of procoagulants, anticoagulants, fibrin(ogen)-binding proteins, molecules,12–20 and metal ions,21,22 as well as contributions of blood and vascular cells, cell-derived microvesicles,23–30 and presence of blood flow31,32 (Figure 2). Many of these mechanisms have been reviewed.33,34.."
source: https://www.ahajournals.org/doi/full...AHA.117.308564
----------------------------------
snip
"Fibrin formation, structure, and stability are regulated by various genetic, biochemical, and environmental factors, allowing for dynamic kinetics of fibrin formation and structure. Interactions between fibrinogen and/or fibrin and plasma proteins and receptors on platelets, leukocytes, endothelial cells, and other cells enable complex functions in hemostasis, thrombosis, pregnancy, inflammation, infection, cancer, and other pathologies. Disorders in fibrinogen concentration and/or function increase risk of bleeding, thrombosis, and infection."
source: https://onlinelibrary.wiley.com/doi/...002/rth2.12191