Fig. 8: Working schematic of how Tsc2 depletion in macrophage aggravated AngII-induced aortic aneurysms formation.
From: Loss of myeloid Tsc2 predisposes to angiotensin II-induced aortic aneurysm formation in mice

Tsc2 depletion enhanced glycolytic activity and upregulated Gpr68 expression in macrophages, resulting in increased transcription activity of CREB. CREB acts on TSP-1, Mmp9 and FOS, aggravating the inflammatory response and elastin degradation, further promoting the formation of AAs.