PKNs are required for cardiac hypertrophy induced by angiotensin II in mice

Angiotensin II induces cardiac hypertrophy in Pkn1/3 double knockout mice, but the response is not sustained by 7 days, unlike wild-type mice.

• Why it matters: The study addresses a gap in whether Pkn1/3 function in adult hearts under pathophysiological stress, where Pkn1/2 have been implicated but Pkn3 remains understudied.
• What they did: Cardiac PKN expression profiles identified PKN2 as dominant and PKN3 largely restricted to endothelial/immune cells; adult wild-type, Pkn1/3DKO, and Pkn2Het mice received 0.8 mg/kg/d AngII with speckle-tracking echocardiography and mRNA/fibrosis readouts.
• The result: AngII increased LV end diastolic mass at 3 days in wild-type and Pkn1/3DKO mice, but further LVEDM growth occurred only in wild-type by 7 days; AngII-linked fibrosis and hypertrophy/matrix mRNAs were suppressed in Pkn1/3DKO mice.