Background: Abdominal aortic aneurysm (AAA) is a chronic degenerative inflammatory
disease. Multi-factors including genetic, environmental and lifestyle factors determine the onsets and
progression of AAAs. Currently surgical repair remains the only effective aneurysm treatment, but no
pharmacological therapy is available for limiting further enlargement of small AAAs and fetal rupture.
Objective: This article is to review our current understanding of angiotensin II (Ang II) and its type 1
receptor (AT1) in AAA pathogenesis as well as the translational potential of AT1 receptor blocker
(ARB) treatment for treating clinical AAA disease.
Results: While many pathways or molecules have been shown to associate with AAA formation and
progression, accumulating evidence indicates the most significant importance of peptide hormone Ang
II and its receptor AT1 in AAA pathogenesis and suggests the translational value of targeting inhibition
of AT1 in treating clinical AAA disease. This review summarized the influences of AT1 deficiency
and pharmacological ARB treatment on experimental AAAs. A discussion has also been made
on whether and how ARB medication in AAA patients changes the natural course of clinical AAAs,
including aneurysm enlargement rate, rupture and AAA-specific mortality. Additionally, we provided
information on two registered clinical trials which are to test the efficacy of telmisartan and valsartan
in limiting small AAA enlargement.
Conclusion: Ang II/AT1 pathway plays a critical role in aneurysmal pathogenesis. Targeting AT1 via
ARB will help establishing novel pharmacological therapies for limiting continuous enlargement of
small AAAs in patients.