Sodium-
glucose co-transporter 2 inhibitors, also known as
gliflozins, were developed as a novel class of anti-diabetic agents that promote
glycosuria through the prevention of
glucose reabsorption in the proximal tubule by
sodium-
glucose co-transporter 2. Beyond the regulation of
glucose homeostasis, they resulted as being effective in different clinical trials in patients with
heart failure, showing a strong cardio-renal protective effect in diabetic, but also in non-diabetic patients, which highlights the possible existence of other mechanisms through which
gliflozins could be exerting their action. So far, different
gliflozins have been approved for their
therapeutic use in T2DM,
heart failure, and
diabetic kidney disease in different countries, all of them being diseases that have in common a deregulation of the inflammatory process associated with the pathology, which perpetuates and worsens the disease. This inflammatory deregulation has been observed in many other diseases, which led the scientific community to have a growing interest in the understanding of the biological processes that lead to or control
inflammation deregulation in order to be able to identify potential therapeutic targets that could revert this situation and contribute to the amelioration of the disease. In this line, recent studies showed that
gliflozins also act as an anti-inflammatory drug, and have been proposed as a useful strategy to treat other diseases linked to
inflammation in addition to cardio-renal diseases, such as diabetes,
obesity,
atherosclerosis, or
non-alcoholic fatty liver disease. In this work, we will review recent studies regarding the role of the main
sodium-
glucose co-transporter 2 inhibitors in the control of
inflammation.