TY - JOUR
T1 - Therapeutic applications of prostaglandins and thromboxane A 2 inhibitors in abdominal aortic aneurysms
AU - Courtois, Audrey
AU - Makrygiannis, Georgios
AU - Cheramy-Bien, Jean Paul
AU - Purnelle, Audrey
AU - Pirotte, Bernard
AU - Dogné, Jean Michel
AU - Hanson, Julien
AU - Defraigne, Jean Olivier
AU - Drion, Pierre
AU - Sakalihasan, Natzi
N1 - This work was supported by the “Fonds pour la chirurgie cardiaque, ASBL” and by the Aneurysmal Pathology Foundation. Courtois A. was funded by the Aneurysmal Pathology Foundation. We thank Betty Nusgens for her comments and corrections during the preparation of this manuscript.
PY - 2018/1/1
Y1 - 2018/1/1
N2 - Background: Abdominal aortic aneurysm (AAA) is one of the leading causes of death in western countries. Surgery is still, at the present time, the sole treatment that has however a significant mortality and cost rate. Many pharmacological agents are under investigation aiming to reduce growth and prevent AAA rupture. These drugs target different pathological pathways and, notably, the excessive production of prostanoids by cyclooxygenases (COX). Intra-aneurysmal thrombus plays an adverse key role in the progression of AAA, platelets being a primary source of prostanoids as thromboxane A2. Objective: In this review, we summarize studies targeting prostanoids production and down-stream pathways in cardiovascular diseases, and more specifically in AAA. Results and Conclusion: Various inhibitors of COX or antagonists of prostanoids receptors have been investigated in AAA animal models with conflicting results. In human AAA, only a few number of studies focused on anti-platelet therapy mostly using acetylsalicylic acid (aspirin, ASA), a COX1 inhibitor. Finally, we report preliminary promising results of a model of AAA in rats receiving a thromboxane A2 inhibitor, BM-573 that induced a reduction of aneurysmal growth.
AB - Background: Abdominal aortic aneurysm (AAA) is one of the leading causes of death in western countries. Surgery is still, at the present time, the sole treatment that has however a significant mortality and cost rate. Many pharmacological agents are under investigation aiming to reduce growth and prevent AAA rupture. These drugs target different pathological pathways and, notably, the excessive production of prostanoids by cyclooxygenases (COX). Intra-aneurysmal thrombus plays an adverse key role in the progression of AAA, platelets being a primary source of prostanoids as thromboxane A2. Objective: In this review, we summarize studies targeting prostanoids production and down-stream pathways in cardiovascular diseases, and more specifically in AAA. Results and Conclusion: Various inhibitors of COX or antagonists of prostanoids receptors have been investigated in AAA animal models with conflicting results. In human AAA, only a few number of studies focused on anti-platelet therapy mostly using acetylsalicylic acid (aspirin, ASA), a COX1 inhibitor. Finally, we report preliminary promising results of a model of AAA in rats receiving a thromboxane A2 inhibitor, BM-573 that induced a reduction of aneurysmal growth.
KW - Abdominal aortic aneurysm
KW - Acetylsalicylic acid
KW - Cyclooxygenase
KW - Platelet
KW - Prostanoids
KW - Thromboxane A2
UR - http://www.scopus.com/inward/record.url?scp=85052234857&partnerID=8YFLogxK
U2 - 10.2174/1389450119666171227224314
DO - 10.2174/1389450119666171227224314
M3 - Review article
C2 - 29749311
AN - SCOPUS:85052234857
SN - 1389-4501
VL - 19
SP - 1247
EP - 1255
JO - Current Drug Targets
JF - Current Drug Targets
IS - 11
ER -