A 70-year-old male with longstanding hypertension develops a thoracic aortic aneurysm. Histology shows 'cystic medial degeneration' with loss of smooth muscle cells and elastic lamina fragmentation. The molecular mediator primarily responsible for elastic tissue destruction is:
- A Neutrophil elastase from infiltrating granulocytes
- B Cathepsin K released from osteoclast-like cells
- C MMP-2 (gelatinase A) and MMP-9 (gelatinase B) degrading elastin and type IV collagen ✓
- D Plasmin generated by tissue plasminogen activator
Explanation
Cystic medial degeneration (medionecrosis) features elastin fragmentation and smooth muscle cell dropout replaced by mucopolysaccharide pools. MMP-2 (constitutively expressed in SMC) and MMP-9 (inducible by angiotensin II, IL-1, and oxidative stress) are the principal matrix metalloproteinases degrading elastin and type IV collagen in the aortic media. TGF-β signaling abnormalities (as in Marfan, Loeys-Dietz syndromes) also activate MMP pathways. Neutrophil elastase causes acute vessel wall injury in aortitis. Cathepsin K is primarily a bone-resorbing enzyme. Plasmin is mainly a fibrin-degrading enzyme.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.