Vascular Aneurysms and Dissections

Marc K Halushka, M. E. Lindsay

Research output: Chapter in Book/Report/Conference proceedingChapter


Aortic aneurysms (AAs) and dissections are rare but important causes of cardiovascular morbidity and mortaLity. Aneurysms can result from genetic predisposition in a MendeLian pattern in the young and old, as well as classical cardiovascular risk factors in older individuals. Despite elastic fiber fragmentation and pools of mucoid material being present in histopathologic specimens, in experimental murine models the causative mechanism for aneurysm progression appears to be altered transforming growth factor beta (TGF-β) activity driving functional deficiencies, rather than a primary structural derangement. Altered TGF-β activity has now been documented in human syndromic aneurysmal disease and in human nonsyndromic aneurysm. This article will describe the diseases and histopathologies of AA. It will also describe the mechanistic alterations in the TGF-β pathway as a result of genetic mutations and how these perturbations inform our understanding of AA development and progression.

Original languageEnglish (US)
Title of host publicationPathobiology of Human Disease
Subtitle of host publicationA Dynamic Encyclopedia of Disease Mechanisms
PublisherElsevier Inc.
Number of pages9
ISBN (Electronic)9780123864567
ISBN (Print)9780123864574
StatePublished - Jan 1 2014


  • Aneurysm
  • Angiotensin
  • Dissection
  • FibrilLin
  • Ghent nosology
  • Loeys-Dietz syndrome
  • Losartan
  • Marfan syndrome
  • Medial degeneration
  • Transforming growth factor beta

ASJC Scopus subject areas

  • Medicine(all)


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