Next Article in Journal / Special Issue
NADPH Oxidase as a Therapeutic Target for Neuroprotection against Ischaemic Stroke: Future Perspectives
Previous Article in Journal / Special Issue
Endovascular Thrombectomy Following Acute Ischemic Stroke: A Single-Center Case Series and Critical Review of the Literature
Article Menu

Export Article

Open AccessReview
Brain Sci. 2013, 3(2), 540-560; doi:10.3390/brainsci3020540

Stroke Neuroprotection: Targeting Mitochondria

1
Department of Cellular and Structural Biology, University of Texas Health Science Center San Antonio, San Antonio, TX 78229, USA
2
Department of Neurology, University of Texas Health Science Center San Antonio, San Antonio, TX 78229, USA
3
Research Imaging Institute, University of Texas Health Science Center San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA
4
School of Medicine, University of Texas Health Science Center San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA
*
Author to whom correspondence should be addressed.
Received: 8 March 2013 / Revised: 8 April 2013 / Accepted: 9 April 2013 / Published: 19 April 2013
(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
View Full-Text   |   Download PDF [958 KB, uploaded 19 April 2013]   |  

Abstract

Stroke is the fourth leading cause of death and the leading cause of long-term disability in the United States. Blood flow deficit results in an expanding infarct core with a time-sensitive peri-infarct penumbra that is considered salvageable and is the primary target for treatment strategies. The only current FDA-approved drug for treating ischemic stroke is recombinant tissue plasminogen activator (rt-PA). However, this treatment is limited to within 4.5 h of stroke onset in a small subset of patients. The goal of this review is to focus on mitochondrial-dependent therapeutic agents that could provide neuroprotection following stroke. Dysfunctional mitochondria are linked to neurodegeneration in many disease processes including stroke. The mechanisms reviewed include: (1) increasing ATP production by purinergic receptor stimulation, (2) decreasing the production of ROS by superoxide dismutase, or (3) increasing antioxidant defenses by methylene blue, and their benefits in providing neuroprotection following a stroke.
Keywords: stroke; purinergic receptor; methylene blue; mitochondria; neuroprotection; superoxide dismutase stroke; purinergic receptor; methylene blue; mitochondria; neuroprotection; superoxide dismutase
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Watts, L.T.; Lloyd, R.; Garling, R.J.; Duong, T. Stroke Neuroprotection: Targeting Mitochondria. Brain Sci. 2013, 3, 540-560.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Brain Sci. EISSN 2076-3425 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top