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Int. J. Mol. Sci. 2018, 19(4), 1211; https://doi.org/10.3390/ijms19041211

Therapeutic Potential of Annexin A1 in Ischemia Reperfusion Injury

1
Department of Molecular & Cellular Physiology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA 71130, USA
2
Department of Neurology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA 71130, USA
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 15 March 2018 / Revised: 3 April 2018 / Accepted: 4 April 2018 / Published: 16 April 2018
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Abstract

Cardiovascular disease (CVD) continues to be the leading cause of death in the world. Increased inflammation and an enhanced thrombotic milieu represent two major complications of CVD, which can culminate into an ischemic event. Treatment for these life-threatening complications remains reperfusion and restoration of blood flow. However, reperfusion strategies may result in ischemia–reperfusion injury (I/RI) secondary to various cardiovascular pathologies, including myocardial infarction and stroke, by furthering the inflammatory and thrombotic responses and delivering inflammatory mediators to the affected tissue. Annexin A1 (AnxA1) and its mimetic peptides are endogenous anti-inflammatory and pro-resolving mediators, known to have significant effects in resolving inflammation in a variety of disease models. Mounting evidence suggests that AnxA1, which interacts with the formyl peptide receptor (FPR) family, may have a significant role in mitigating I/RI associated complications. In this review article, we focus on how AnxA1 plays a protective role in the I/R based vascular pathologies. View Full-Text
Keywords: ischemia–reperfusion injury; Annexin A1; formyl peptide receptors; ischemic stroke ischemia–reperfusion injury; Annexin A1; formyl peptide receptors; ischemic stroke
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Ansari, J.; Kaur, G.; Gavins, F.N.E. Therapeutic Potential of Annexin A1 in Ischemia Reperfusion Injury. Int. J. Mol. Sci. 2018, 19, 1211.

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