Metalloproteinase and stroke infarct size: Role for anti-inflammatory treatment?

132Citations
Citations of this article
101Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Deregulation of matrix metalloproteinases (MMPs), the largest class of human proteases, has been implicated in brain damage in both animal and human studies. Some MMPs are elevated after stroke (both in plasma and in brain tissue), and their expression is enhanced by t-PA during thrombolysis related to hemorrhagic transformation events. Although the exact cellular source of MMPs remains unknown, brain endothelium, astrocytes, neurons, and inflammatory-activated cells, such as neutrophils, may release MMP-2, MMP-3, MMP-8, MMP-9, MMP-10, and/or MMP-13. Neurovascular perturbations occurring after stroke lead to blood-brain barrier leakage, edema, hemorrhage, leukocyte infiltration, and progressive inflammatory reactions to brain injury over hours or even days after the initial stroke. Synthesized MMP inhibitors and several compounds used for stroke secondary prevention, such as anti-inflammatory drugs, might decrease MMPs and improve the acute treatment of human brain ischemia without compromising the beneficial effects of matrix plasticity during stroke recovery. © 2010 New York Academy of Sciences.

Cite

CITATION STYLE

APA

Morancho, A., Rosell, A., García-Bonilla, L., & Montaner, J. (2010). Metalloproteinase and stroke infarct size: Role for anti-inflammatory treatment? Annals of the New York Academy of Sciences, 1207, 123–133. https://doi.org/10.1111/j.1749-6632.2010.05734.x

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free