Impact of beta-myosin heavy chain expression on cardiac function during stress
Why the study?
A shift from alpha- to beta-MHC occurs in failing hearts, but its impact on disease progression and cardiac function under chronic stress is not well understood.
Does a pre-existing shift from alpha- to beta-MHC affect cardiac function under chronic mechanical or pharmacologic cardiovascular stress in mice?
Population
Transgenic mice with replacement of alpha- with beta-MHC and non-TG mice
Comparison
Beta-MHC transgenic mice vs non-transgenic mice under chronic mechanical or pharmacologic cardiovascular stress
Design
Transgenic animal study
Key result
Transgenic expression of beta-MHC in mice resulted in augmented LV hypertrophy, decompensation, and accelerated dilation under severe cardiovascular stress compared to non-transgenic mice.
Authors
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Hypothesis-generating only; leaves open MHC isoform modulation as a HF target.
Does a pre-existing shift from alpha- to beta-MHC affect cardiac function under chronic mechanical or pharmacologic cardiovascular stress in mice?
The shift from alpha- to beta-myosin heavy chain isoform observed in cardiac disease appears to be a maladaptive response that worsens cardiac function under severe cardiovascular stress.
Krenz et al. (2004) studied Cardiovascular stress. Transgenic beta-myosin heavy chain (beta-MHC) expression vs. Non-transgenic mice was evaluated on Cardiac function and ventricular morphology under stress. Transgenic expression of beta-MHC in mice resulted in augmented LV hypertrophy, decompensation, and accelerated dilation under severe cardiovascular stress compared to non-transgenic mice.