A 65-year-old man with a 6.5 cm infrarenal abdominal aortic aneurysm (AAA) undergoes repair. Pathology of the aortic wall shows thinning and fragmentation of elastic lamellae with marked infiltration of lymphocytes, macrophages, and plasma cells in the adventitia, plus increased MMP (matrix metalloproteinase) expression. Which MMPs are MOST responsible for elastin and collagen degradation in AAA pathogenesis?
- A MMP-1 (collagenase) and MMP-3 (stromelysin)
- B MMP-2 (gelatinase A) and MMP-9 (gelatinase B) ✓
- C MMP-7 (matrilysin) and MMP-11
- D MMP-13 (collagenase 3) and MMP-14 (MT-MMP)
Explanation
AAA formation is driven by MMP-mediated elastolysis and collagenolysis. MMP-9 (gelatinase B/collagenase IV) and MMP-2 (gelatinase A) are the principal proteases that degrade elastin and denatured collagen (gelatin) in the aortic media and adventitia. Macrophages and neutrophils in adventitial inflammation secrete MMP-9, while smooth muscle cells contribute MMP-2. These enzymes, when not adequately counterbalanced by TIMPs (tissue inhibitors of metalloproteinases), progressively destroy the structural integrity of the aortic wall. MMP-9 levels correlate with AAA expansion rate. Other contributing factors include oxidative stress, autoimmune adventitial inflammation, and smoking (the strongest risk factor for AAA).
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
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