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HIF1α in aortic aneurysms and beyond
Author(s) -
Tomoki Hashimoto,
Victor Rizzo
Publication year - 2017
Publication title -
clinical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.91
H-Index - 138
eISSN - 1470-8736
pISSN - 0143-5221
DOI - 10.1042/cs20160956
Subject(s) - abdominal aortic aneurysm , extracellular matrix , limiting , hypoxia (environmental) , aortic aneurysm , medicine , transcription factor , disease , aneurysm , microbiology and biotechnology , cardiology , cancer research , surgery , biology , gene , chemistry , genetics , mechanical engineering , organic chemistry , oxygen , engineering
Abdominal aortic aneurysm (AAA) is a permanent expansion of the vessel wall with a high prevalence in those 65 years of age and older. Aneurysms are prone to dissection and rupture that carry a mortality rate of over 85%. Currently, surgical repair is the only option to treat this disease. The need to intervene prior to these events has set off a flurry of basic studies in an effort to understand the cellular and molecular mechanisms that govern AAA formation, progression and rupture. In the present study, the role of myeloid cells in contributing to AAA development has been confirmed. More specifically, the transcription factor, hypoxia-inducible factor-1α (HIF1α), was demonstrated to be a necessary component for regulating the expression of extracellular matrix modifying enzymes and their endogenous inhibitors in these cells. This new discovery may lead to therapeutic targets to prohibit the degradation and weakening of the vessel wall with the hope of limiting AAA formation and/or growth.

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