Key result
In mice with transaortic constriction, PDE5 overexpression worsened cardiac dysfunction and hypertrophy by functionally retargeting PDE5 to hydrolyze natriuretic peptide-derived cGMP.
Why the study?
Does PDE5 retargeting alter cGMP signaling and contribute to pathological cardiac hypertrophy in mice subjected to transaortic constriction?
Does PDE5 retargeting alter cGMP signaling and contribute to pathological cardiac hypertrophy in mice subjected to transaortic constriction?
In pathological cardiac hypertrophy, PDE5 functionally retargets to hydrolyze natriuretic peptide-derived cGMP, suppressing protective protein kinase G activity and worsening cardiac remodeling.
No takes yet. Share an insight, caveat, or question.
PDE5 retargeting may suppress protective cGMP signaling in hypertrophy; hypothesis-generating for human therapies without clinical validation.
Zhang et al. (2012) studied Pathological Cardiac Hypertrophy. PDE5 overexpression (P5+) and transaortic constriction vs. Controls and N3(-) mice was evaluated on Cardiac dysfunction, hypertrophy, and cGMP signaling. In mice with transaortic constriction, PDE5 overexpression worsened cardiac dysfunction and hypertrophy by functionally retargeting PDE5 to hydrolyze natriuretic peptide-derived cGMP.
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