N.A. Loginova1, N.V. Panov2
1,2 Institute of Higher Nervous Activity and Neurophysiology of the Russian Academy of Sciences (Moscow, Russia)
1 loginova@ihna.ru, 2 nikolay.panov1966@yandex.ru
Impaired cerebral microcirculation affects both neurovascular units (a complex of neurons and vessel surfaces interacting via astrocytes) and the extracellular matrix (ECM). The extracellular matrix is a complex network with a heterogeneous structure composed of polysaccharides and proteins. It includes substances that remodel it, as well as receptors through which extracellular matrix components interact with cells.
Aim of the work – to analyze the contribution of the extracellular matrix to the maintenance of nervous tissue homeostasis and the development of pathologies associated with impaired cerebral blood supply.
Extracellular matrix is not just a passive scaffold but an active regulator of nervous tissue homeostasis and a key participant in the pathogenesis of cerebral ischemia. Components of the basement membrane (collagen type IV, laminin, perlecan) and the perineuronal network (hyaluronic acid, chondroitin sulfate and heparan sulfate proteoglycans) ensure the integrity of the blood–brain barrier and the function of the neurovascular unit. In ischemia, including the photochemical thrombosis model, degradation of the extracellular matrix by matrix metalloproteinases (MMP‑2, ‑9, ‑13), changes in integrin expression, decreased perlecan levels, as well as fibrosis and neuroinflammation occur. ECM remodeling affects microglial and astrocytic migration, glial scar formation, and the severity of post‑ischemic damage.
Understanding the role of the extracellular matrix in cerebral ischemia opens new therapeutic targets. The use of matrix metalloproteinase inhibitors can arrest basement membrane destruction and reduce blood–brain barrier permeability. The results of the study can be used to develop strategies aimed at preserving extracellular matrix integrity and modulating integrin signaling to improve post‑stroke recovery.
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