Fig. 6: Partial improvement in trajectories of obesity-induced gene expression changes in heart, lung, kidney and brain ECs by a reversion diet. | Nature Metabolism

Fig. 6: Partial improvement in trajectories of obesity-induced gene expression changes in heart, lung, kidney and brain ECs by a reversion diet.

From: Single-cell profiling of vascular endothelial cells reveals progressive organ-specific vulnerabilities during obesity

Fig. 6

a, Changes in the gene expression levels of AP1 transcription factor subunits in arteriole ECs in obesity and reversion conditions. b, DEGs associated with ECM organization, including Col4a1, Col4a2, Col15a1 and Nrp2, in cardiac cap ECs. c, Gene expression changes in Klf genes in cardiac art, cap and ven ECs of obese and reversion animals. d, Quantification of the EC-pneumocyte population as a proportion of all lung ECs. e, MSigDB-curated pathways upregulated in obesity in lung cap ECs (adjusted P value of <0.05 and log (FC) > 0.1), which show improved trajectory in the diet reversion group. f, Expression levels of select inflammation-associated genes upregulated in lung cap and art ECs in obesity. g, Gene expression changes in members of the fourth mitochondrial respiratory chain complex in the aEC population. h, Gene expression changes in AP1 transcription factor subunits in kidney art, cap and ven ECs of obese and reversion animals. i, Differential expression of genes encoding mitochondrial respiration subunits in the kidney mEC2 population. Select genes are indicated. Data were standardized to the chow control group at each timepoint. j, BioPlanet-annotated pathways upregulated in brain cap ECs in obesity (adjusted P value of <0.05 and log (FC) > 0.1), showing an improved trajectory in the reversion group. k, Expression of select leukocyte adhesion genes in brain art ECs. Adjusted P values in e and j indicate adjustments for multiple comparisons using the Benjamini–Hochberg method.

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