Extended Data Fig. 2: Atherosclerosis development relies on GLS1-dependent glutaminolyis.

(a) Metabolic pathway (left) and RNAseq analysis (right) of Apoe^−/− versus WT mouse aortas (6 weeks on WD) performed with Phantasus software (GSE10000). Red indicates up- and blue down-regulated expression. (b) Oil red O staining (left) or ¹⁴C glutamine accumulation after i.v. injection (right) in descending aortas extracted from female WT and Apoe^−/− mice maintained on a WD for 6 weeks. (c) ¹⁴C glutamine incorporation in aortas obtained from female Apoe^−/− and Apoe^−/− Mac^∆Gls1 mice fed for 6 weeks on WD. (d) Cholesterol (left) and triglyceride (right) content in plasma of Apoe^−/− and Apoe^−/− Mac^∆Gls1 mice. (e) Representative sections (left) and quantification (right) of aortic plaques from Apoe^−/− or Apoe^−/− HSC^∆Gls1 mice (12 weeks WD) stained for Oil Red O and Hematoxylin Eosin. Scale bar: 200 μm. (f) Representative sections (top) and quantification (bottom) of aortic plaques from Apoe^−/− or Apoe^−/− Mac^∆Gls1 mice (12 weeks WD) stained for CD68 and Ki67. (g) Gating strategy (left) and quantification (right) of PCM efferocytic index in Apoe^−/− and Apoe^−/− Mac^ΔGls1 mice 1-hour after labeled ACs i.p. injection. Both sexes were analyzed. All values are mean ± SEM and are representative of at least one independent experiment (n = 4 independent animals for c, n = 7 to 9 for e-g). P values were determined by a two-tailed Student’s t-test. Source data are provided as a Source Data file (c-g).

Source data