Fig. 5: Improved trajectories of ECM components in AT ECs and of metabolic and inflammatory networks in liver ECs in the reversion group.
a, Changes in the proportion of angiogenic and proliferating ECs in visceral AT and subcutaneous AT in WD-treated and reversion cohorts. Data are presented relative to chow controls at each timepoint. b, GO cellular component pathways upregulated in AT cap ECs in obesity, which switch toward chow levels in the reversion group. c, Gene expression changes in focal adhesion genes in cap ECs in visceral and subcutaneous AT. d, Gene expression changes in fatty acid transporters in art, cap and ven ECs in the visceral and subcutaneous AT. e, DEGs (adjusted P value of <0.05 and | log (FC) | > 0.1) in hepatic cap ECs at the 6-month timepoint. Genes that show a restored transcriptional profile in the reversion group are indicated. f, BioPlanet-annotated pathways upregulated in cap ECs in obesity (adjusted P value of < 0.05 and log (FC) > 0.1), which are restored toward chow levels in the reversion group. g, Expression of Vcam1, Icam1, Cxcl9 and Cxcl10 in WD and reversion groups in liver cap ECs. h, BioPlanet-annotated pathways downregulated in hepatic cap ECs in obesity (adjusted P value of <0.05 and log (FC) < 0.1), which are restored toward healthy chow levels in the reversion group. i, Gene expression changes in fatty acid transporters in liver art, cap and ven ECs. j, Expression of Apoc1, Apoa2, Apoc3 and Ldlr in WD and reversion groups in liver cap ECs. k, UMAPs showing coexpression of endothelial markers (Pecam1 and Flt1) and platelet markers (Pf4, Ppbp and Nrgn) in the liver EC-platelet population, which is marked by the black arrow. l, Percentage of ECs positive for Pf4, Ppbp or Nrgn in liver in chow, WD and reversion cohorts at each timepoint. The adjusted P value indicates adjustments for multiple comparisons using the Benjamini–Hochberg method (b, f and h).
