In summary, the study reveals how sepsis-induced lactate production activates endothelial cells and promotes ferroptosis through H3K14 lactylation, ultimately leading to vascular injury and lung ...

This state is mediated by a receptor on endothelial cells called Tie2. Under normal conditions, ANGPT2 prompts Tie2 to produce an anti-inflammatory response. However, these conditions are reversed ...

To find out, the researchers created mice lacking STIM1 in endothelial cells, and in a series of experiments, compared these mice to normal mice exposed to the sepsis toxin. They found that ...

The scientists found that the antibody against β1-integrin bound to the vascular endothelium, improved the junctions between endothelial cells and decreased vascular leakage in sepsis.

Sometimes also called septic shock, this condition is caused ... The lactate latches on to endothelial cells in the bone marrow; for the first time, the researchers identified a special lactate ...

Endothelial progenitor cells derived from bone marrow are believed ... 23 from cardiovascular causes (4.5 percent); other causes included sepsis (9 patients), chronic renal insufficiency (3 ...

The general pathology involves increased permeability of the endothelial cells of the pulmonary capillary and of the epithelial cells of the alveoli. Sepsis induced ARDS is often caused by ...

The reason for organ failure in sepsis patients is because the endothelial cells lining blood vessels become leaky, resulting in abnormal fluid shifts which ultimately shut down the blood supply.

APC, via the protein C pathway, is a natural homeostatic regulator with multiple mechanisms of action, making it a unique modulator of vascular function at the endothelial cell and leukocyte ...