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Renal denervation attenuates cardiac hypertrophy in spontaneously hypertensive rats via regulation of autophagy

机译:肾脏去神经支配通过自噬调节减轻自发性高血压大鼠的心脏肥大

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摘要

It has been suggested that renal denervation (RD) may attenuate left ventricular (LV) hypertrophy. However, the role that autophagy serves in this process is currently unclear. In the present study, utilizing a model of hypertension-induced cardiac hypertrophy in spontaneous hypertensive rats, it was demonstrated that RD was significantly associated with a reduction in LV hypertrophy. Furthermore, a decrease in the myocardial mRNA of hypertrophy-associated genes was demonstrated in RD rats compared with sham controls. In addition, RD in hypertension-induced LV hypertrophy rats was associated with the attenuation of cellular autophagic response over activation at a physiological level. This was indicated by a reduction in the expression of Beclin-1, autophagy related 9A and microtubule-associated protein 1A/1B-light chain 3 II/I in RD rats to physiological levels that are observed in control rats. Furthermore, the number of autophagosomes was restored to physiological levels in the cardiomyocytes of RD rats. The results of the current study suggest that RD may attenuate LV hypertrophy via the regulation of autophagic responses.
机译:已经提出,肾神经支配(RD)可以减轻左心室(LV)肥大。但是,目前尚不清楚自噬在此过程中的作用。在本研究中,利用自发性高血压大鼠的高血压诱发的心脏肥大模型,证明RD与LV肥大的减少显着相关。此外,与假对照组相比,在RD大鼠中证实了肥大相关基因的心肌mRNA的减少。此外,在生理水平上,高血压诱发的左室肥大大鼠的RD与细胞自噬反应减弱有关。这通过RD大鼠中Beclin-1,自噬相关9A和微管相关蛋白1A / 1B-轻链3 II / I的表达降低至对照大鼠中观察到的生理水平来表明。此外,在RD大鼠的心肌细胞中,自噬体的数目恢复到生理水平。目前的研究结果表明,RD可能通过调节自噬反应来减轻LV肥大。

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