Figure 2. ITGAM deficiency attenuates the development of experimental AAA, vascular structural injury, and the inflammatory response.

A, Representative photographs of the infrarenal abdominal aortas in saline‐ or CaCl₂‐treated WT and ITGAM(‐/‐) male mice. The black dotted lines indicate the edge of abdominal aortas. B, Kaplan–Meier survival curves of WT (n=15) and ITGAM(‐/‐) mice (n=15). No significant difference was found regarding the survival rate. C, Incidence of AAA formation in WT and ITGAM(‐/‐) mice in response to CaCl₂. D, Maximal abdominal aortic diameter of WT (n=15) and ITGAM(‐/‐) mice (n=13) 6 weeks after being exposed to CaCl₂ and the sham‐treated mice (n=15). The data represent the mean±SEM. **P<0.01, ***P<0.001. E, Representative H&E, EVG, and Masson trichrome staining of the abdominal aortic tissues from the sham‐treated, WT, and ITGAM(‐/‐) mice. Scale bar=100 μm. F and G, Quantification of elastin fragmentation and collagen deposition in the experimental groups (n=6), *P<0.05, **P<0.01, ****P<0.0001. H through K, Serum CCL2, TNF‐α, IL‐6, and IL‐1β levels in the experimental groups (n=6 for each group) detected by ELISA, *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. AAA indicates abdominal aortic aneurysm; EVG, Elastica Van Gieson; H&E, hematoxylin and eosin; ITGAM, integrin subunit alpha M; and WT, wild‐type.