that preventing miR-133a interacting with IP3RII mRNA increased production of the IP3 receptorcausinghypertrophy in cardiomyocytes
pressure overloading(passive) may be caused byPathologic hypertrophy
alterations in calcium homeostasis and mechanical stretch with resultant transcriptional activation ( 2–4(passive) may be triggered byPathologic hypertrophy
Recently , transfection of an antisense nucleotide to MAPK was shownto preventhypertrophy in cardiomyocytes
changes in enzymatic action ,promptshypertrophy of hepatocytes
nih.gov ) Stimulation of cultured cardiac myocytes in vitro with isoproterenol ( ISO ) , an agonist for beta(1)- and beta(2)-ARscausedhypertrophy of myocytes
prostaglandin ) F2α , one of the primary prostanoids generated in the vascular tissuecauseshypertrophy of VSMCs
to heart failure and death , discovering ERK1/2 's downstream targets and precisely how it controls the hypertrophic responsecan leadto heart failure and death , discovering ERK1/2 's downstream targets and precisely how it controls the hypertrophic response
on the other handcauseson the other hand
to the compromise of both diastolic and systolic function , which can be regarded as a result of volume or pressure overload or other hormonal or cytokine stimulicould contributeto the compromise of both diastolic and systolic function , which can be regarded as a result of volume or pressure overload or other hormonal or cytokine stimuli
to decreased organ function and , ultimately , organ failure ; andcontributesto decreased organ function and , ultimately , organ failure ; and
if left uncheckedcould leadif left unchecked
negative remodeling of the ventricles and often extreme concentric or eccentric hypertrophy whereas exercise typically produces a mild 10 - 20 % growth of the ventricles in a uniform manner 1,2causesnegative remodeling of the ventricles and often extreme concentric or eccentric hypertrophy whereas exercise typically produces a mild 10 - 20 % growth of the ventricles in a uniform manner 1,2