Background: Aortic aneurysms (AAs) are without effective pharmacologic
therapy, in clinical usage, in part because of the limited understanding of
factors leading to AA development.
Objective: The objectives of this study were to examine the evidence that cigarette
smoking induces AAs through altering matrix metalloproteinases (MMP) and the
molecular biology/pharmacology that maybe involved in this effect.
Methods: A systematic search was conducted to identify studies that examined the
links between cigarette smoke, MMP and AAs.
Results: Eleven studies were identified. There was consistency, between studies.
They found that cigarette smoke, nicotine or tobacco products increased aortic dimension and the proportion
of AAs. Nicotine and tobacco constituents induced MMPs: MMP-1, MMP-2, MMP-8, MMP-9
and MMP-12 but with different levels of consistency. The molecular mechanisms involved in the
pathogenesis of cigarette-induced AA formation, ranked according to the consistency of evidence include
JNK, AMPK-2, Jak Stat, and mTOR/p70Sk and PTEN pathways.
Conclusion: Nicotine and tobacco constituents translate the exposure to cigarette smoke into increased
MMP expression through various molecular mechanisms whose interruption can form the basis for
pharmacologic management of AAs.