Stroke; a journal of cerebral circulation
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Comparative Study
Key role of CD36 in Toll-like receptor 2 signaling in cerebral ischemia.
Toll-like receptors (TLRs) and the scavenger receptor CD36 are key molecular sensors for the innate immune response to invading pathogens. However, these receptors may also recognize endogenous "danger signals" generated during brain injury, such as cerebral ischemia, and trigger a maladaptive inflammatory reaction. Indeed, CD36 and TLR2 and 4 are involved in the inflammation and related tissue damage caused by brain ischemia. Because CD36 may act as a coreceptor for TLR2 heterodimers (TLR2/1 or TLR2/6), we tested whether such interaction plays a role in ischemic brain injury. ⋯ In the brain, TLR2/1 signaling requires CD36. The cooperative signaling of TLR2/1 and CD36 is a critical factor in the inflammatory response and tissue damage evoked by cerebral ischemia. Thus, suppression of CD36-TLR2/1 signaling could be a valuable approach to minimize postischemic inflammation and the attendant brain injury.
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It is unknown how little flow velocity improvement is necessary to achieve recanalization and clinical recovery. We sought to investigate which flow velocity parameter was associated with complete recanalization/reperfusion and neurological improvement in patients receiving reperfusion therapies. ⋯ A modest increase in the EDV as opposed to peak systolic velocity is associated with complete recanalization/reperfusion, early neurological improvement, and favorable functional outcome. Diastolic flow augmentation may represent a novel target for development of reperfusion therapies.