The Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitor Empagliflozin Reverses Hyperglycemia-Induced Monocyte and Endothelial Dysfunction Primarily through Glucose Transport-Independent but Redox-Dependent Mechanisms.
Dilvin SemoJulius ObergasselMarc DorenkampPia HemlingJasmin StrutzUrsula HidenNicolle MüllerUlrich Alfons MüllerSajan Ahmad ZulfikarRinesh GodfreyJohannes WaltenbergerPublished in: Journal of clinical medicine (2023)
This study provides data indicating the beneficial role of empagliflozin in reversing hyperglycaemia-induced vascular cell dysfunction. Even though both monocytes and endothelial cells express functional SGLT-2, SGLT-2 is not the primary glucose transporter in these cells. Therefore, it seems likely that empagliflozin does not directly prevent hyperglycaemia-mediated enhanced glucotoxicity in these cells by inhibiting glucose uptake. We identified the reduction of oxidative stress by empagliflozin as a primary reason for the improved function of monocytes and endothelial cells in hyperglycaemic conditions. In conclusion, empagliflozin reverses vascular cell dysfunction independent of glucose transport but could partially contribute to its beneficial cardiovascular effects.
Keyphrases
- endothelial cells
- oxidative stress
- high glucose
- induced apoptosis
- diabetic rats
- blood glucose
- single cell
- cell cycle arrest
- dendritic cells
- signaling pathway
- cell therapy
- peripheral blood
- endoplasmic reticulum stress
- dna damage
- cell death
- stem cells
- bone marrow
- drug induced
- machine learning
- immune response
- big data
- blood pressure
- insulin resistance
- type diabetes
- stress induced