European Journal of Molecular & Clinical Medicine

Abstract

Acute ischemic damage to neurons during the development of a focus of cerebral infarction (CI) is based on a complex cascade of interaction between the endothelium of the vascular wall, hemostatic factors, neurons and microglia. Oxygen starvation of tissues stimulates the production of endothelial cells of endothelial dysfunction markers produced by blood vessel endotheliocytes, macrophages, neurons and neuroglia in response to hypoxic brain damage. The so-called “cell death genes” are activated, which are responsible for the development of apoptosis, or programmed death of ischemic penumbra cells, as a result of the expansion of which the infarction volume increases