الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Myocardial hypertrophy is a compensatory mechanism for an increased workload as in pregnancy, or in pathological conditions as hypertension. However, it is considered a predictor of cardiovascular morbidity and mortality as it can lead to overt HF and sudden death.
The animal model of cardiac hypertrophy induced by ISO is one of the widely accepted and well-defined hypertrophic models which is characterized by technical simplicity, excellent reproducibility, and an acceptable level of mortality.
TLM is an ARB that is widely used in the treatment of hypertension, congestive HF, and diabetic nephropathy. Experimental evidence suggested that AT1 activation induces fibroblast proliferation and myocyte hypertrophy while antagonizing its effects has shown significant benefits in preventing fibrosis-elicited HF.
TMZ is a metabolic anti-ischemic agent, which increases the tolerance of cardiomyocytes to ischemia. However, few studies have explored the effect of TMZ on ventricular remodeling in patients with LVH. TMZ is likely to improve left ventricular remodeling, symptoms of angina and myocardial ischemia.
Autophagy appears to play dual roles in myocardial hypertrophy. Many reports have suggested that the high level of autophagy plays a beneficial role in cardiac hypertrophy, while other studies show deleterious functions of autophagy in myocardial hypertrophy. Therefore, autophagy may play adaptive or maladaptive roles in the pathologic process of cardiac hypertrophy depending on the conditions and the extent of stimulation.
Previous studies have discussed the role of TLM or TMZ in myocardial hypertrophy, but -to the best of our knowledge- none explored the role of their combination in preventing myocardial hypertrophy. The current study for the first time examined the effect of TLM/TMZ combination and the role of autophagy as a mechanism of the preventive effects produced by TLM and TMZ in ISO-induced myocardial hypertrophy in rats.