Canagliflozin and myocardial oxidative stress: SGLT1 inhibition takes centre stage
Abstract
This editorial refers to ‘Effects of canagliflozin on human myocardial redox signalling: clinical implications’, by H. Kondo et al., http://dx.doi:10.1093/eurheartj/ehab420. Sodium–glucose co-transporter type 2 inhibitors (SGLT2is), also known as gliflozins, are a recently discovered class of oral antidiabetic drugs.1 SGLT2is promote urinary glucose excretion through inhibition of SGLT2 and SGLT1, which are responsible for ∼90% and 10% of glucose reabsorption in the kidney glomerulus respectively. Although gliflozins show variable affinity for SGLT2 over SGLT1—with empagliflozin being the most selective SGLT2i followed by dapagliflozin, canagliflozin, and sotagliflozin—inhibition of SGLT2 has become eponymous with this class of drugs, as glucose transport is the primary site of the intended use of these agents, i.e. blood glucose lowering.2 In 2015, the EMPA-REG OUTCOME (Empagliflozin Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients) trial reported improved cardiovascular outcomes in patients with type 2 diabetes (T2D) treated with empagliflozin.3...
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