Fig. 1: Impact of Ang II-induced hypertension on the cardiovascular proteome of male and female WT and ANXA1^-/- mice.

Proteomics preparation and analysis workflow of TA (n = 4–5) and LV (n = 4–5) (A). Created in Biorender. Singh, J (2025) https://creativecommons.org/licences/by/3.0/. Significantly upregulated (red/purple) and downregulated (blue/green) cellular components in TA (B and E) and LV (H and K). Distribution of identified proteins (Venn) displaying proteins identified in TA (co-identified proteins: center, non-bold and significantly changed proteins: center, bold) and volcano plot indicating differential abundance of proteins associated with structural (red), calcium regulatory (orange), inflammatory (green), oxidative stress (purple), and mitochondrial (blue) networks in TA of normotensive and hypertensive WT (C, D) and ANXA1^-/- (F, G) mice of both sexes. Venn diagram comparing the LV proteome (co-identified proteins: center, non-bold and significantly changed proteins: center, bold) and volcano plot indicating differential abundance of proteins associated with structural (red), calcium regulatory (orange), inflammatory (green), oxidative stress (purple), and mitochondrial (blue) proteins in LV of normotensive and hypertensive WT (I, J) and ANXA1^-/- (L, M) mice of both sexes. Fold change of proteins with P < 0.05 (calculated with Student’s t test) was considered statistically significant. Ang II: angiotensin II, ANXA1^-/-: annexin-A1-deficient, GO: gene ontology annotation, LV: left ventricle, Sal: saline, TA: thoracic aorta, WT: wild-type.