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Pathophysiology of Ischemic Stroke

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Translational Research in Stroke

Part of the book series: Translational Medicine Research ((TRAMERE))

Abstract

In this chapter, we summarize the characteristics of pathophysiological changes after ischemic stroke. Ischemic stroke is a rapid occurring and developing disease, which is caused by one or several cerebral artery occlusions. The occlusion could be due to the thrombus or thrombosis. The immediate change after ischemic stroke includes ion balance destroyed such as Na+–K+ pump dysfunction, calcium overload, acid-sensing ion channel opening, and peri-infarct depolarization. The following change is metabolism failure such as decrease of ATP and pH levels, increase of excitotoxicity response, reduced protein synthesis, and disturbed phosphatase activity. After then, free radical release, inflammatory response, apoptosis, necrosis, autophagy, and blood-brain barrier disruption could occur based on the duration and severity of ischemia. During this process, the body defense system could be activated, and angiogenesis, neurogenesis, and oligodendrogenesis could simultaneously be induced. Finally, we also discuss briefly how to manage ischemic brain injury based on the pathophysiological changes.

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Abbreviations

3-MA:

3-Methyladenine

AIF:

Apoptosis-inducing factor

AMPARs:

Amino-3-hydroxy-5-methyl-4-isoxanole propionate receptors

ASICs:

Acid-sensing ion channels

Bax:

Bcl-2-associated X protein

BBB:

Blood-brain barrier

Bcl-2:

B-cell lymphoma 2

Bid:

BH3 Interacting-domain death agonist

CaMKII:

Ca2+/calmodulin-dependent protein kinase II

DAPK1:

Death-associated protein kinase 1

DCE-MRI:

Dynamic contrast-enhanced magnetic resonance imaging

Drp1:

Dynamin-related protein 1

EndoG:

Endonuclease G

LC3-II:

Microtubule-associated light chain 3 II protein

LMP:

Lysosomal membrane permeabilization

MMPs:

Matrix metalloproteinases

mPTP:

Mitochondrial permeability transition pore

NCXs:

Na+-Ca2+ exchangers

NMDARs:

N-Methyl-D-aspartate receptors

nNOS:

Neuronal nitric oxide synthase

PARP-1:

Poly(ADP-ribose) polymerases-1

PSD-95:

Postsynaptic density-95 protein

PUMA:

p53-upregulated modulator of apoptosis

ROS:

Reactive oxygen species

Smac:

Second mitochondria-derived activator of caspase

SUMOylation:

Small ubiquitin-like modifier conjugation

tMCAO:

Transient middle cerebral artery occlusion

TNF-α:

Tumor necrosis factor-α

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Authors and Affiliations

  1. Department of Neurology, Shanghai Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, China

    Yongfang Li

  2. Med-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, 1954 Hua Shan Road, Shanghai, 200030, China

    Guo-Yuan Yang

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  1. Yongfang Li
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  1. Department of Neurology & Neurosurgery, Cedars-Sinai Medical Center, Advanced Health Sciences Pavilion, Los Angeles, California, USA

    Paul A. Lapchak

  2. Med-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China

    Guo-Yuan Yang

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Li, Y., Yang, GY. (2017). Pathophysiology of Ischemic Stroke. In: Lapchak, P., Yang, GY. (eds) Translational Research in Stroke. Translational Medicine Research. Springer, Singapore. https://doi.org/10.1007/978-981-10-5804-2_4

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