Apelin-deficient (APL‑KO) mice develop increased aortic stiffness and hypertension through extracellular matrix remodeling. Deficiency alters adipose tissue secretome, elevates protease (cathepsin S, neutrophil elastase) activity, leading to collagen (type I/III) accumulation and elastic fiber fragmentation in the aortic wall, raising pulse wave velocity (PWV) and mean arterial pressure.
Apelin loss causes adipose inflammation; ECM remodeling in aorta (collagen deposition, elastolysis); elevated PWV and systemic hypertension; increased cathepsin S activity mediates elastic fiber fragmentation
Apelin Knockout mouse (Apelin⁻/⁻) — genOway‑developed, C57BL/6 background
Vascular stiffening; arterial hypertension; ECM remodeling; adipokine role; obesity-linked vascular pathology
Homologous recombination targeting Apln in ES cells; Apelin^–/– constitutive Knockout; phenotyping via PWV, blood pressure tail cuff; histological collagen/elastin assays; adipose secretome protease activity
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