ArticleFrontiers in neurology2026
Brain cell-released Cyclophilin A induces neuroinflammation and exacerbates blood-brain barrier injury in acute ischemic stroke.
Article in Frontiers in neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Excessive neuroinflammation mediates blood-brain barrier (BBB) disruption and poor outcomes after acute ischemic stroke (AIS). Cyclophilin A (CypA), when released into the extracellular space (designated as eCypA), may participate in inflammatory reactions and vascular dysfunction. However, its role in regulating neuroinflammation and BBB injury in AIS, as well as the therapeutic potential of targeting eCypA remain unclear. Methods: ELISA was used to detect eCypA release in serum from 22 AIS patients (17 mild, 5 severe; 13 males, 9 females; mild: age 65.41 ± 10.20 years, NIHSS 2.88 ± 1.45; severe: age 64.00 ± 5.04 years, NIHSS 9.40 ± 3.29; blood sampled within 48 h of onset), in serum/cerebrospinal fluid (CSF) from transient middle cerebral artery occlusion (tMCAO) rats, and in supernatants from BV2 (microglia) or bEnd.3 (brain microvascular endothelial cells) exposed to oxygen-glucose deprivation/reoxygenation (OGD/R) or lipopolysaccharide (LPS). Nine-week-old male Sprague-Dawley rats ( Results: eCypA levels were significantly elevated in AIS patient serum (1.74 ± 0.23 ng/mL in mild, 2.39 ± 0.09 ng/mL in severe vs. 1.30 ± 0.19 ng/mL in healthy controls, Conclusion: eCypA, released by microglia and brain microvascular endothelial cells under ischemic-hypoxic and inflammatory conditions, serves as a critical pathogenic mediator that drives neuroinflammation and BBB disruption in AIS. Targeting eCypA with C46 peptide effectively abrogates these pathological cascades, thereby supporting eCypA as a novel therapeutic target for AIS.
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