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The ischemic cascade, triggered by the blockage of oxygenated blood supply to brain tissue, leads to excitotoxicity, oxidative stress, inflammation, and eventually, cell death. Current research highlights the promising neuroprotective effects of conditioning, which induces ischemic tolerance (IT). Thus, the main objective of this study is to analyze selected genes affected by ischemic stroke and the neuroprotective response to ischemic stroke, with a focus on ischemia and ischemic tolerance in peripheral blood. We investigated changes in gene expression indicative of cerebral ischemia during carotid endarterectomy (CEA), a procedure that involves the temporary occlusion of the\n                      <jats:italic>arteria carotis interna<\/jats:italic>\n                      . To assess the influence of CEA on IT induction, we performed a whole-transcriptome analysis of peripheral blood cells isolated from symptomatic (791 DEGs in correlation with negative control), asymptomatic (688 DEGs in correlation with negative control), and oximetric (637 DEGs in correlation with negative control) patients. The presence of gene expression changes in genes selectively identified through whole-transcriptome analysis was subsequently statistically verified. Using quantitative qRT-PCR, we monitored gene expression changes in10 genes\n                      <jats:italic>SLC2A14, TRPM7, UGP2, PLLP, ND4L, HMSD, SESN3, DPY19L4, UBE3A,<\/jats:italic>\n                      and\n                      <jats:italic>PCDH9<\/jats:italic>\n                      . The results suggest that CEA affected the expression of all monitored genes, with statistically significant differences between groups, indicating the activation of distinct ischemic tolerance cascades in different patient groups. These findings may contribute to a better understanding and characterizing of the molecular mechanisms underlying ischemic tolerance.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s12031-025-02470-0","type":"journal-article","created":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T10:18:49Z","timestamp":1770113929000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Potential Protective Effect of Carotid Endarterectomy: Inducing Ischemic Tolerance in Brain Tissue after Stroke"],"prefix":"10.1007","volume":"76","author":[{"given":"Rastislav","family":"Mucha","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marek","family":"Furman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexandra","family":"Urbanova","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivan","family":"Kopolovets","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miroslava","family":"Nemethova","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michal","family":"Virag","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stanislav","family":"Hresko","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vladimir","family":"Katuch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vladimir","family":"Sihotsky","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,2,3]]},"reference":[{"key":"2470_CR1","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2024.1344039","volume":"12","author":"M Albaik","year":"2024","unstructured":"Albaik M, Sheikh Saleh D, Kauther D, Mohammed H, Alfarra S, Alghamdi A, Ghaboura N, Sindi IA (2024) Bridging the gap: glucose transporters, Alzheimer\u2019s, and future therapeutic prospects. 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