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Protective effects of Gα<sub>i3</sub> deficiency in a murine heart-failure model of β<sub>1</sub>-adrenoceptor overexpression.


ABSTRACT: We have shown that in murine cardiomyopathy caused by overexpression of the β1-adrenoceptor, Gαi2-deficiency is detrimental. Given the growing evidence for isoform-specific Gαi-functions, we now examined the consequences of Gαi3 deficiency in the same heart-failure model. Mice overexpressing cardiac β1-adrenoceptors with (β1-tg) or without Gαi3-expression (β1-tg/Gαi3-/-) were compared to C57BL/6 wildtypes and global Gαi3-knockouts (Gαi3-/-). The life span of β1-tg mice was significantly shortened but improved when Gαi3 was lacking (95% CI: 592-655 vs. 644-747 days). At 300 days of age, left-ventricular function and survival rat

SUBMITTER: Schroper T 

PROVIDER: S-EPMC10933181 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature