Key result
IGF-I lowered I(K) and I(K1) activities, and inhibition of MAPKs or Akt alleviated these effects, suggesting K+ channels are regulated dichotomically by acutely stimulated MAPKs and Akt.
Basal I(K) and I(K1) are positively maintained by steady-state Akt and ERK activities, and eccentric cardiac hypertrophy shifts the regulation of steady-state basal activities of K+ channels towards MAPKs.
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Rat myocyte data on IGF-I/K+ channel regulation via MAPKs/Akt are hypothesis-generating; leaves open translation to human eccentric hypertrophy.
Teos et al. (2008) studied Eccentric cardiac hypertrophy. IGF-I and specific inhibitors for ERK1/2, p38 MAPK, and PI3K/Akt vs. Sham / normal hearts was evaluated on I(K) and I(K1) activities. IGF-I lowered I(K) and I(K1) activities, and inhibition of MAPKs or Akt alleviated these effects, suggesting K+ channels are regulated dichotomically by acutely stimulated MAPKs and Akt.
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