Therapeutic potential of annexin A1 in ischemia reperfusion injury

Research output: Contribution to journalReview article

Authors

External Institution(s)

  • LSU Health Sciences Center - Shreveport

Details

Original languageEnglish (US)
Article number1211
JournalInternational journal of molecular sciences
Volume19
Issue number4
StatusPublished - Apr 16 2018
Peer-reviewedYes

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.

    Research areas

  • Annexin A1, Formyl peptide receptors, Ischemia-reperfusion injury, Ischemic stroke

Citation formats

APA

Ansari, J., Kaur, G., & Gavins, F. N. E. (2018). Therapeutic potential of annexin A1 in ischemia reperfusion injury. International journal of molecular sciences, 19(4), [1211]. https://doi.org/10.3390/ijms19041211

Harvard

Ansari, J, Kaur, G & Gavins, FNE 2018, 'Therapeutic potential of annexin A1 in ischemia reperfusion injury', International journal of molecular sciences, vol. 19, no. 4, 1211. https://doi.org/10.3390/ijms19041211