Key result
Dual loss of RGS2 and 5 in male mice led to 75% mortality within 72-96 hours after surgery-induced stress, alongside increased arrhythmias and disrupted Gi/o signaling.
Why the study?
Whether RGS2 and 5 redundantly control G protein signaling to maintain cardiovascular homeostasis was unknown.
Population
Rgs2/5 dbKO and WT mice and isolated cardiomyocytes
Comparison
Dual absence of RGS2 and 5 (Rgs2/5 dbKO) vs WT
Design
Preclinical animal and cellular experimental study
Authors
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Dual RGS2/5 deletion effects in mice leave open redundant GPCR control of cardiac homeostasis; human relevance requires prospective validation.
RGS2 and RGS5 redundantly promote normal ventricular rhythm by coordinating Gi/o signaling and facilitating cardiomyocyte calcium handling.
Dahlen et al. (2022) studied Ventricular myocyte arrhythmias and cardiovascular homeostasis. Dual loss of RGS2 and 5 (Rgs2/5 dbKO) vs. Wild-type (WT) mice was evaluated on Mortality after surgery-induced stress. Dual loss of RGS2 and 5 in male mice led to 75% mortality within 72-96 hours after surgery-induced stress, alongside increased arrhythmias and disrupted Gi/o signaling.
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