Key result
FGF-2 deficiency in mice resulted in dilated cardiomyopathy and a failure to develop compensatory cardiac hypertrophy in response to Angiotensin II-induced hypertension.
Why the study?
Does FGF-2 deficiency impair Angiotensin II-induced cardiac hypertrophy in mice?
Population
Mice deficient in FGF-2 expression and wild-type mice
Comparison
Angiotensin II-dependent hypertension model vs Wild-type mice subjected to the same Ang II model
Design
Preclinical
Authors
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No immediate clinical implications; leaves open FGF-2 as a hypertrophy modulator pending translational studies.
Does FGF-2 deficiency impair Angiotensin II-induced cardiac hypertrophy in mice?
FGF-2 of fibroblast origin is a crucial mediator of compensatory cardiac hypertrophy via autocrine/paracrine actions on cardiac cells.
Pellieux et al. (2001) studied Angiotensin II-dependent hypertension and cardiac hypertrophy. FGF-2 deficiency vs. Wild-type mice was evaluated on Cardiac hypertrophy and MAPK activation. FGF-2 deficiency in mice resulted in dilated cardiomyopathy and a failure to develop compensatory cardiac hypertrophy in response to Angiotensin II-induced hypertension.
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