The development of innovative drug therapy in aortic dissection

2014 Fiscal Year Final Research Report

• Project/Area Number: 25861236
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Cardiovascular surgery
• Research Institution: Kurume University
• Principal Investigator: NISHIDA Norifumi 久留米大学, 医学部, 助教 (50624508)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 大動脈解離 / ピオグリタゾン / 塩分過剰 / IL-17

Outline of Final Research Achievements

In this project, we investigated whether pioglitazone suppresses aortic dissection. Unexpectedly, pioglitazone worsened the aortic dissection in mice. We hypothesized that sodium retention by pioglitazone might be the underlying mechanism. In fact, excessive sodium intake worsened aortic dissection through IL-17 pathway. Transcriptome analysis of aortae before the onset of aortic dissection showed strong induction of proinflammatory genes and suppression of extracellular matrix genes. Deletion of IL-17 gene resulted in the augmented expression of extracellular matrix genes and enhanced collagen deposition. From these results, we concluded that IL-17 suppresses the extracellular matrix synthesis, which in turn worsens aortic dissection. We will continue to explore the mechanism of aortic dissection, focussing on the roles of IL-17 and extracellular matrix.

Free Research Field

血管外科、分子血管病態学