CaM kinase signaling induces cardiac hypertrophy and activates the MEF2 transcription factor in vivo
Population
Cardiomyocytes in vitro and transgenic mice overexpressing CaMKIV and/or constitutively activated NFAT3
Design
Preclinical
Authors
Discussion
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Implication
Hypothesis-generating for CaMKIV-MEF2 in hypertrophy; leaves open human relevance and therapeutic targeting.
Key Points
- This study aims to explore the role of CaM kinase signaling in cardiac hypertrophy and its effects on the MEF2 transcription factor.
- In vivo analysis of CaMKI and CaMKIV function in hypertrophy of transgenic mice.
- Assessment of left ventricular end-diastolic diameter and fractional shortening in CaMKIV overexpressing mice.
- Investigation of the interaction between CaMK signaling and NFAT3 in inducing hypertrophy.
- CaMKIV overexpression resulted in increased left ventricular end-diastolic diameter (specific measurements not stated) and decreased fractional shortening.
- Activated CaMKIV induced hypertrophic cardiomyocyte responses both in vitro and in vivo.
- CaMKIV was found to activate MEF2 more efficiently than calcineurin, suggesting distinct roles in the hypertrophic response.
Structured PICO
P
Population
Cardiomyocytes in vitro and transgenic mice overexpressing CaMKIV and/or constitutively activated NFAT3
I
Intervention
Activation and overexpression of Ca(2+)/calmodulin-dependent protein kinases-I and -IV (CaMKI and CaMKIV)
O
Outcome
Cardiac hypertrophy (including increased left ventricular end-diastolic diameter, decreased fractional shortening, and MEF2 activation)surrogate
CaMK signaling induces cardiac hypertrophy by activating the MEF2 transcription factor, acting synergistically and in parallel with the calcineurin/NFAT pathway.
Cite This Study
Passier et al. (2000) studied this question.