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Su. Neuroimmunol Neuroinflammation 2017;4:260-2 Neuroimmunology and
DOI: 10.20517/2347-8659.2017.22
Neuroinflammation

www.nnjournal.net
Topic: Stroke Open Access

Inflammation and genetic factors in stroke

pathogenesis

Hua Su

Center for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, CA 94143, USA.
Correspondence to: Dr. Hua Su, Center for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California,
San Francisco, 1001 Potrero Avenue, Box 1363, San Francisco, CA 94143, USA. E-mail: hua.su@ucsf.edu
How to cite this article: Su H. Inflammation and genetic factors in stroke pathogenesis. Neuroimmunol Neuroinflammation 2017;4:260-2.

Article history: Received: 29 Apr 2017 First Decision: 9 Jun 2017 Revised: 10 Jun 2017 Accepted: 13 Jun 2017 Published: 8 Dec 2017

Stroke is the leading cause of serious, long- is positively correlated with the survival rate of stroke
term disability in the United States. Each year, patients. In addition, increased angiogenesis was
approximately 795,000 people suffer a stroke. About associated with an improved functional outcome after
600,000 of these are first attacks, and 185,000 are ischemic stroke in both animal models and in stroke
recurrent attacks. Nearly three-quarters of all strokes patients. However, despite considerable research
occur in people over the age of 65 (www.strokecenter. efforts, the exact mechanisms for stroke injury have
org/patients/about-stroke/stroke-statistics/). According not been fully understood. None of neuroprotection
to the American Stroke Association, stroke is the 5th and angiogenesis strategies has shown therapeutic
leading cause of death in the United States, killing benefit in clinical setting. Administration of intravenous
130,000 every year. The prevalence of stroke and recombinant tissue plasminogen activator (rtPA) is
its cost will undoubtedly rise as the aging population still the only effective treatment. The therapeutic
increases. In addition, stroke incidence and mortality window of rtPA is limited within 4.5 h after the onset of
are increasing in less developed countries in which ischemic stroke [1,2] . Endovascular treatment has been
the lifestyles and population restructuring are rapidly shown to improve functional outcome in 5 randomized
changing. clinical trials on selected patients with acute ischemic
stroke. Thrombectomy with stent retrievers is now
After ischemic stroke, severe disturbance of the blood recommended as the standard of care for acute
supply to brain tissue deprives oxygen supply to brain ischemic strokes with a proximal large vessel occlusion
tissue causing neuronal death. Pathophysiological in the anterior circulation. However, the therapeutic
[1]
events occur after ischemic stroke include ionic window for this treatment is also limited .
imbalance, neuroinflammation, excitotoxicity, activity
of microglia. All of these contribute to neuronal Cerebral ischemia induces a cascade of inflammatory
death. Ischemia induces a significant increase in and immune reactions that encompass genomic as well
microvascular density, a sign of angiogenesis, in as molecular and cellular events. Immune response
the penumbra of the cerebral infarct. The degree of has been shown to play a major role in ischemic stroke
increased vessel-density in the ischemic penumbra progression. The extent of neuronal damage seems to

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