Intraventricular hemorrhage (IVH) occurs in 15% to 40% of preterm births and is frequently associated with long‐term neurological deficits. The rupture of the proliferative germinal zone following IVH disturbs the late production of neurons, ependymal cells, and glial cells.
The pro‐inflammatory molecule Galectin‐3 (Gal‐3), which is frequently increased in cancer and injury, regulates inflammation and subventricular zone (SVZ) neurogenesis; however, the signaling pathways involved remain poorly understood.
Adult neurogenesis contributes to neurological function; therefore, elucidating the underlying molecular mechanisms in post‐stroke neurogenesis could provide for the development of new therapies to amplify endogenous neurogenesis and improve neurological function during recovery.
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