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Endothelial inflammation in COVID-19
Endothelial inflammation in COVID-19

The vascular endothelium, which normally maintains blood flow and resists clotting and inflammation, can become overactive during COVID-19.

This overactivation can lead to multiorgan complications and long-term effects associated with Long Covid.

“Disrupted endothelial function underlies the multiorgan complications of COVID-19”

Disrupted endothelial function underlies the multiorgan complications of COVID-19
·science.org·
Endothelial inflammation in COVID-19
SARS-CoV-2 infection of human pluripotent stem cell-derived vascular cells reveals smooth muscle cells as key mediators of vascular pathology during infection
SARS-CoV-2 infection of human pluripotent stem cell-derived vascular cells reveals smooth muscle cells as key mediators of vascular pathology during infection

Using stem-cell-derived vascular cells, researchers found SARS-CoV-2 infects smooth muscle cells (SMCs), not endothelial cells.

Infected SMCs cause inflammation and clotting factors, explaining vascular issues seen in severe COVID-19 cases.

·biorxiv.org·
SARS-CoV-2 infection of human pluripotent stem cell-derived vascular cells reveals smooth muscle cells as key mediators of vascular pathology during infection
Persistent endothelial dysfunction in post-COVID-19 syndrome and its associations with symptom severity and chronic inflammation
Persistent endothelial dysfunction in post-COVID-19 syndrome and its associations with symptom severity and chronic inflammation

Long Covid patients exhibited persistent endothelial dysfunction.

This was indicated by lower venular flicker-induced dilation (vFID), narrower central retinal artery equivalent (CRAE), and lower arteriolar-venular ratio (AVR).

“Our results demonstrate that prolonged endothelial dysfunction is a hallmark of PCS, and impairments of the microcirculation seem to explain ongoing symptoms in patients.”

·link.springer.com·
Persistent endothelial dysfunction in post-COVID-19 syndrome and its associations with symptom severity and chronic inflammation
Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis
Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis
“Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis”
Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis
·medrxiv.org·
Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis
Unraveling Covid’s Pernicious Role in Brain Fog and Clotting
Unraveling Covid’s Pernicious Role in Brain Fog and Clotting

“Navigating social distancing requirements that complicated lab work, Akassoglou and her collaborators conducted a series of experiments in mice to explore the pernicious role of the coronavirus’s spike protein.

They discovered that beyond serving as the virus’s “key” to enter cells, spike binds with a blood clotting factor called fibrinogen, creating structurally abnormal, inflammation-promoting clumps of fibrin — the insoluble material that forms the mesh-like structures essential for wound healing.

High levels of these abnormal clots not only push the body’s clotting system into overdrive, increasing clot formation and inflammation, but also suppress natural killer cells — the immune system’s virus-clearing soldiers.”

Navigating social distancing requirements that complicated lab work, Akassoglou and her collaborators conducted a series of experiments in mice to explore the pernicious role of the coronavirus’s spike protein. They discovered that beyond serving as the virus’s “key” to enter cells, spike binds with a blood clotting factor called fibrinogen, creating structurally abnormal, inflammation-promoting clumps of fibrin — the insoluble material that forms the mesh-like structures essential for wound healing. High levels of these abnormal clots not only push the body’s clotting system into overdrive, increasing clot formation and inflammation, but also suppress natural killer cells — the immune system’s virus-clearing soldiers.
·bloomberg.com·
Unraveling Covid’s Pernicious Role in Brain Fog and Clotting
SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels
SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels

Autopsy study in patients with COVID shows that: SARS-CoV-2 infects, replicates and persists in Macrophages within the coronary vasculature Since CARDIAC MACROPHAGES have a half-life of 8.8years they would act as VIRAL RESERVOIRS in Atherosclerotic plaques

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels
·nature.com·
SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels
No Amount of Hand-Washing Can Make COVID-19 a Seasonal Virus
No Amount of Hand-Washing Can Make COVID-19 a Seasonal Virus

No Amount of Hand-Washing Can Make COVID-19 a Seasonal Virus

"The selection of words modulates the message...terms such as “seasonal”, “like a cold”, and “like the flu” can be selected by writers to...lull the reader into a false sense of security... COVID-19 is not primarily a respiratory infection. This virus can cause a systemic disease with far-reaching effects on the body, particularly blood vessels. Once SARS-CoV-2 enters the body, the virus can affect the ...blood vessels, causing inflammation and damage.

·x.com·
No Amount of Hand-Washing Can Make COVID-19 a Seasonal Virus