Induction of cardiac fibulin-4 protects against pressure overload-induced cardiac hypertrophy and heart failure.

ABSTRACT: The prevailing view of fibulin-4 deficient mice is that the cardiac phenotype is the result of aortic and/or valvular disease. In the present study, we have tested whether the cardiac phenotype is, at least in part, the consequence of primary cardiac effects of fibulin-4. We have found fibulin-4 expression to be activated throughout the myocardium in wildtype (fibulin-4^+/+) C57Bl/6J;129 Sv mice subjected to transverse aortic constriction (TAC). In contrast, haploinsufficient fibulin-4^+/R mice exposed to severe TAC do not show this increase in myocardial fibulin-4 expression, but display altered physical properties of myocardial tissue. Moreover, TAC-induced cardiac fibrosis, pulmonary congestion, and mortality are aggravated in fibulin-4^+/R mice. In vitro i

SUBMITTER: van Deel ED 

PROVIDER: S-EPMC12022050 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature