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. Author manuscript; available in PMC: 2026 Oct 23.
Published in final edited form as: Cell. 2026 Oct 8;189(21):6792–6809.e21. doi: 10.1016/j.cell.2026.09.032

Figure 2. Gimap6 deficiency synergizes with hyperlipidemia to drive lethal coronary atherosclerosis in Ldlr−/− mice.

Figure 2.

(A) Kaplan-Meier survival curves of SFD-fed Ldlr−/−, Gimap6+/−Ldlr−/−, Gimap6−/−, and Gimap6−/−Ldlr−/− mice (males/females, n = 34/33, 36/33, 67/60, and 21/26). Gimap6−/− data are replotted from Figure 1A.

(B, C) En face ORO staining (B) and plaque quantification (C) in Ldlr−/− and Gimap6−/−Ldlr−/− mice fed SFD or switched to HFD at 8 weeks and analyzed after 12 or 8 weeks for male and females, respectively. (n = 5 per sex and genotype). Scale bars, 0.5 cm.

(D, E) Masson’s trichrome staining (D) and CD68, α-SMA, and DAPI immunofluorescence staining (E) of aortae from male Ldlr−/− and Gimap6−/−Ldlr−/− mice after 12 weeks of HFD. Red arrows mark foam cells; black arrows mark necrotic cores; dashed yellow lines mark the smooth muscle layer; white arrows indicate macrophage infiltration. Scale bars, 250 μm.

(F, G) Masson’s trichrome staining (F) and quantification (G) of aortic valve plaque and necrotic core areas from Ldlr−/− and Gimap6−/−Ldlr−/− mice after 4 weeks of HFD (males/females, n = 3/3 and 3/4, respectively). Scale bars, 200 μm.

(H) Histological analysis of intramyocardial coronary arteries from HFD-challenged female Ldlr−/− and Gimap6−/−Ldlr−/− mice from (B). Masson’s trichrome (columns 1–3), ORO (column 4), and CD68/α-SMA/DAPI immunofluorescence (column 5). Bottom panels show enlarged views. Scale bars, 100 μm.

Statistics: log-rank (A); two-way ANOVA (C, G). See also Figures S2-S5.

Unless otherwise indicated, data are mean ± SD. Statistical significance is denoted as ns, not significant; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.