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Emerging research employed lentivirus-mediated shRNA to knock down GLP-1R expression in vitro, resulting in diminished effects of GLP-1RAs on mitochondrial function by day 21, along with impaired mitochondrial autophagy and autophagic clearance
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It was initially postulated to be a compensatory mechanism to the blood pressure lowering effect of GLP-1 RAs that was possibly mediated by their vasodilatory effect [9, 31] and/or increased urinary sodium excretion [32]
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