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Pericytes in Ischemic Stroke

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Pericyte Biology in Disease

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 1147))

Abstract

Recent stroke research has shifted the focus to the microvasculature from neuron-centric views. It is increasingly recognized that a successful neuroprotection is not feasible without microvascular protection. On the other hand, recent studies on pericytes, long-neglected cells on microvessels have provided insight into the regulation of microcirculation. Pericytes play an essential role in matching the metabolic demand of nervous tissue with the blood flow in addition to regulating the development and maintenance of the blood–brain barrier (BBB), leukocyte trafficking across the BBB and angiogenesis. Pericytes appears to be highly vulnerable to injury. Ischemic injury to pericytes on cerebral microvasculature unfavorably impacts the stroke-induced tissue damage and brain edema by disrupting microvascular blood flow and BBB integrity. Strongly supporting this, clinical imaging studies show that tissue reperfusion is not always obtained after recanalization. Therefore, prevention of pericyte dysfunction may improve the outcome of recanalization therapies by promoting microcirculatory reperfusion and preventing hemorrhage and edema. In the peri-infarct tissue, pericytes are detached from microvessels and promote angiogenesis and neurogenesis, and hence positively effect stroke outcome. Expectedly, we will learn more about the place of pericytes in CNS pathologies including stroke and devise approaches to treat them in the next decades.

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Acknowledgments

Dr. Turgay Dalkara’s research is supported by The Turkish Academy of Sciences. Dr. Luis Alarcon-Martinez prepared Figs. 9.1a and 9.6.

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Correspondence to Turgay Dalkara .

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Dalkara, T., Alarcon-Martinez, L., Yemisci, M. (2019). Pericytes in Ischemic Stroke. In: Birbrair, A. (eds) Pericyte Biology in Disease. Advances in Experimental Medicine and Biology, vol 1147. Springer, Cham. https://doi.org/10.1007/978-3-030-16908-4_9

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