Effects of Global Ripk2 Genetic Deficiency in Aged Mice following Experimental Ischemic Stroke.

ABSTRACT: Besides the loss of blood and oxygen reaching the ischemic tissue, many secondary effects of ischemic stroke can cause additional tissue death, including inflammation, oxidative stress, and proteomic disturbances. Receptor-interacting serine/threonine kinase 2 (RIPK2) is an important mediator in the post-stroke inflammatory cascade that responds to signals and molecular patterns released by dead or dying cells in the ischemic area. We hypothesize that RIPK2 signaling worsens injury and neurological recovery post-stroke and that global deletion of Ripk2 will be protective following ischemic stroke in aged mice. Aged (18-24 months) male mice were subjected to permanent middle cerebral artery occlusion (pMCAO). Vertical grid, weight grip, and open field were conducted at baseline and o

SUBMITTER: Howell JA 

PROVIDER: S-EPMC11839111 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature