Anti-Inflammation and Anti-Oxidation: The Key to Unlocking the Cardiovascular Potential of SGLT2 Inhibitors and GLP1 Receptor Agonists.
Veronika A MyasoedovaMichele BozziVincenza ValerioDonato MoschettaIlaria MassaiuValentina RusconiDaniele Di NapoliMichele CiccarelliValentina ParisiPiergiuseppe AgostoniStefano GenovesePoggio PaoloPublished in: Antioxidants (Basel, Switzerland) (2023)
Type 2 diabetes mellitus (T2DM) is a prevalent and complex metabolic disorder associated with various complications, including cardiovascular diseases. Sodium-glucose co-transporter 2 inhibitors (SGLT2i) and glucagon-like peptide 1 receptor agonists (GLP1-RA) have emerged as novel therapeutic agents for T2DM, primarily aiming to reduce blood glucose levels. However, recent investigations have unveiled their multifaceted effects, extending beyond their glucose-lowering effect. SGLT2i operate by inhibiting the SGLT2 receptor in the kidneys, facilitating the excretion of glucose through urine, leading to reduced blood glucose levels, while GLP1-RA mimic the action of the GLP1 hormone, stimulating glucose-dependent insulin secretion from pancreatic islets. Both SGLT2i and GLP1-RA have shown remarkable benefits in reducing major cardiovascular events in patients with and without T2DM. This comprehensive review explores the expanding horizons of SGLT2i and GLP1-RA in improving cardiovascular health. It delves into the latest research, highlighting the effects of these drugs on heart physiology and metabolism. By elucidating their diverse mechanisms of action and emerging evidence, this review aims to recapitulate the potential of SGLT2i and GLP1-RA as therapeutic options for cardiovascular health beyond their traditional role in managing T2DM.
Keyphrases
- blood glucose
- glycemic control
- rheumatoid arthritis
- cardiovascular events
- type diabetes
- cardiovascular disease
- disease activity
- blood pressure
- coronary artery disease
- ankylosing spondylitis
- insulin resistance
- weight loss
- heart failure
- signaling pathway
- metabolic syndrome
- atrial fibrillation
- adipose tissue
- nitric oxide
- human health
- binding protein
- drug induced