Endothelial CXCL5 negatively regulates myelination and repair after white matter stroke

Xiao, Guanxi; Kumar, Rosie; Burguet, Jasmine; Komuro, Yutaro; Kakarla, Visesha; Williams, CK; Xr, Zhang; Macknicki, Michal; Brumm, Andrew J; Kawaguchi, Riki; Vinters, H.V.; Carmichael, S. Thomas; La, Havton; DeCarli, Charlie S.; Jd, Hinman

doi:10.1101/664953

Cited by 1 publication

(1 citation statement)

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“…48 In a chronic injury model, animals on a high-fat diet demonstrate increased perivascular oligodendrocyte progenitor cells with the association driven by IL-17 signaling. 49 Rajani et al 50 demonstrated that endothelial dysfunction driven by a mutation in Atp11b increases endothelial production of HSP90α (heat shock protein 90 alpha) that inhibits the maturation of oligodendrocytes. The role of intercellular inflammatory signaling in stroke and white matter injury is just beginning to be explored but holds significant promise as an anti-inflammatory therapeutic strategy for vascular brain health.…”

Section: Inflammatory Pathways Driving Chronic Cerebrovascular Diseasementioning

confidence: 99%

Inflammation and the Link to Vascular Brain Health: Timing Is Brain

Mun

Hinman

2022

Stroke

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Inflammation and its myriad pathways are now recognized to play both causal and consequential roles in vascular brain health. From acting as a trigger for vascular brain injury, as evidenced by the coronavirus disease 2019 (COVID-19) pandemic, to steadily increasing the risk for chronic cerebrovascular disease, distinct inflammatory cascades play differential roles in varying states of cerebrovascular injury. New evidence is regularly emerging that characterizes the role of specific inflammatory pathways in these varying states including those at risk for stroke and chronic cerebrovascular injury as well as during the acute, subacute, and repair phases of stroke. Here, we aim to highlight recent basic science and clinical evidence for many distinct inflammatory cascades active in these varying states of cerebrovascular injury. The role of cerebrovascular infections, spotlighted by the severe acute respiratory syndrome coronavirus 2 pandemic, and its association with increased stroke risk is also reviewed. Rather than converging on a shared mechanism, these emerging studies implicate varied and distinct inflammatory processes in vascular brain injury and repair. Recognition of the phasic nature of inflammatory cascades on varying states of cerebrovascular disease is likely essential to the development and implementation of an anti-inflammatory strategy in the prevention, treatment, and repair of vascular brain injury. Although advances in revascularization have taught us that time is brain, targeting inflammation for the treatment of cerebrovascular disease will undoubtedly show us that timing is brain.

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Section: Inflammatory Pathways Driving Chronic Cerebrovascular Diseasementioning

confidence: 99%