TIMPing the Aorta
Smooth Muscle Cell–Specific Deletion of BMAL1 Limits Murine Abdominal Aortic Aneurysm Development
Abdominal aortic aneurysms (AAAs) are defined as enlargements of the abdominal aorta to >1.5-fold of their normal size (usually around 3 cm).1 The overall AAA prevalence is estimated to be 6% in men and 1.6% in women.2 The asymptomatic and silent nature of an aneurysm makes their diagnosis extremely challenging, whereas ruptured AAAs account for ≈15 000 deaths in the United States annually.3 Until now only surgical (open or endovascular) repair exist as treatment options for patients. A better understanding of the subcellular deregulations and regulatory networks triggering aneurysm expansion seem of essential importance for the discovery of novel therapeutic targets.
See accompanying article on page 1063
Homeostasis of vascular smooth muscle cells (VSMCs), being the major component of the vasculature, plays a crucial—but controversial—role in AAA development and disease progression. Although VSMCs contribute to aortic inflammation and synthesis of MMPs (matrix metalloproteinases), their proliferation and production of matrix proteins has stabilizing effects.4 Loss of VSMCs through apoptosis is overall considered detrimental for aneurysm progression.
In this current issue of ATVB, …