Key result
MEKK1 deficiency in mice subjected to cardiac pressure overload did not prevent cardiac hypertrophy but resulted in significantly increased myocyte apoptosis (1.50 vs 0.44 myocytes/mm2) and higher mortality.
Why the study?
Does MEKK1 deficiency affect pressure overload-induced cardiac hypertrophy, apoptosis, and heart failure in mice?
Does MEKK1 deficiency affect pressure overload-induced cardiac hypertrophy, apoptosis, and heart failure in mice?
Absolute Event Rate: 1.5% vs 0.44%
p-value: p=0.02
MEKK1 is required for pressure overload-induced JNK activation and protects against apoptosis and heart failure, but is dispensable for the development of cardiac hypertrophy.
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MEKK1 may protect against apoptosis and mortality in pressure overload without affecting hypertrophy; hypothesis-generating for its therapeutic targeting in human HF.
Sadoshima et al. (2002) studied Pressure overload-induced cardiac hypertrophy (n=34). MEKK1 deficiency vs. Wild-type (MEKK1+/+) was evaluated on TUNEL-positive myocytes in LV myocardium at 7 days (myocytes/mm2) (p=0.02). MEKK1 deficiency in mice subjected to cardiac pressure overload did not prevent cardiac hypertrophy but resulted in significantly increased myocyte apoptosis (1.50 vs 0.44 myocytes/mm2) and higher mortality.
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