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Volume 37 Issue 9
Sep.  2010
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Article Contents

TGF-β signaling in aortic aneurysm: another round of controversy

doi: 10.1016/S1673-8527(09)60078-3
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  • Corresponding author: E-mail address: linfuyu2000@yahoo.com.cn (Fuyu Lin); E-mail address: yangx@nic.bmi.ac.cn (Xiao Yang)
  • Received Date: 2010-04-20
  • Accepted Date: 2010-06-08
  • Rev Recd Date: 2010-05-28
  • Available Online: 2010-10-07
  • Publish Date: 2010-09-20
  • Aortic aneurysm (AA) is a common health problem with high mortality and no effective drugs. Transforming growth factor-β (TGF-β) superfamily members regulate various cellular processes, and TGF-β signaling has key roles in development, tissue homeostasis, and diseases. Interest in the role of TGF-β signaling in the pathogenesis of AAs has recently emerged, particularly since genetic studies demonstrated an association between gene mutations in components of TGF-β signaling and AAs. However, paradoxical discoveries have implicated dysregulated TGF-β signaling in aneurysm formation, complicating the precise functional role for TGF-β in aneurysm development and progression. Furthermore, interventions targeting towards TGF-β signaling using losartan, which may represent a suitable therapeutic option for AAs, were subject to skepticism especially because of conflicting experimental results obtained from TGF-β antibody treatment without knowledge of the underlying mechanism. We propose a TGF-β aneurysm paradox, which would provide a good opportunity for the development of genetic mouse models of AA. These models would be used to clarify the mechanisms underlying TGF-β signaling, which would translate into novel pharmacologic therapies based on the new molecular discoveries.
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