Fig. 4. Effects of sex difference on human and MCT rat right ventricular remodeling associated with pulmonary hypertension.
a, Number of patients in each group, separated by sex, and the Fisher’s exact test P value for compensated-versus-decompensated RV and normal-versus-PAH RV pairs. b, Schematic of RV dysfunction in male and female participants, which shows a different route (longer) for female decompensated RV failure compared with males. Differentially enriched pathways in male compensated and decompensated RV samples and female decompensated RV demonstrate independent biological routes of maladaptive RV remodeling in female and male PAH participants. c, Regulation of 116 differentially regulated genes associated with estrogen and progesterone metabolism (FDR < = 0.05) in all human RV samples. n (normal RV) = F:5, M:8, n (compensated RV) = F:10, M:3, n (decompensated RV) = F:9, M:4. Colors represent the scaled gene expression (rows, z-score). d, Hemodynamics assessment of MCT rats RV functions for male and female animals. n (cRV male) = 5, n (dRV male) = 6, n (cRV female) = 7, n (dRV female) = 3, n (control F, M) = 4. Data are presented as the mean ± s.e.m. P value was calculated by one-way analysis of variance (ANOVA) followed by Tukey’s multiple-comparisons test. e,f, Genes and pathways that were specifically regulated in male (e) and female (f) decompensated RV samples, respectively. g, Schematic of RV remodeling in MCT-induced rat model, highlighting the main differentially regulated pathways in male and female animals (green, upregulated; orange, downregulated). cRV, compensated right ventricle; dRV, decompensated right ventricle; M, male; F, female; RVSP, right ventricle systolic pressure; CO, cardiac output; BW, body weight; NS, not significant.