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Intriguingly, in other organ systems, SLGT2 inhibitors also appear to drive changes that are potentially relevant to skeletal muscle dysfunction, for example, increasing lipolysis and ketogenesis, reducing inflammatory cytokines in liver [153], the aforementioned reduction in RAAS activity [154] and upregulation of AMPK via the sestrin pathway with consequent inhibition of mTOR in cardiac myocytes [153]

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The primary endpoint was the incidence of MACEs (cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, hospitalization for heart failure)