Ca2+/Calmodulin-dependent Kinase II and Calcineurin Play Critical Roles in Endothelin-1-induced Cardiomyocyte Hypertrophy

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Population

Cultured cardiac myocytes of neonatal rats

Comparison

Endothelin-1 stimulation with or without CaMKII… vs Control (unstimulated or ET-1 alone)

Design

Preclinical

Authors

Discussion

Hypothesis-generating for CaMKII/calcineurin inhibition in hypertrophy; requires in vivo and human validation before any clinical consideration.

Population

Cultured cardiac myocytes of neonatal rats

Intervention

Endothelin-1 (ET-1) stimulation with or without CaMKII and calcineurin inhibitors (KN62, cyclosporin A) or dominant-negative mutants

Comparator

Control (unstimulated or ET-1 alone)

Outcome

beta-MHC promoter activation, [(3)H]phenylalanine uptake, and cell sizesurrogate

Ca2+ plays a critical role in ET-1-induced cardiomyocyte hypertrophy by activating CaMKII- and calcineurin-dependent pathways.

Zhu et al. (2000) studied this question.

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Hypothesis-generating for CaMKII/calcineurin inhibition in hypertrophy; requires in vivo and human validation before any clinical consideration.