Gao 2022 EBioMedicine

Gao YM, Feng ST, Wen Y, Tang TT, Wang B, Liu BC (2022) Cardiorenal protection of SGLT2 inhibitors-Perspectives from metabolic reprogramming. EBioMedicine 83:104215. https://doi.org/10.1016/j.ebiom.2022.104215

» PMID: 35973390 Open Access

Gao YM, Feng ST, Wen Y, Tang TT, Wang B, Liu BC (2022) EBioMedicine

Abstract: Sodium-glucose co-transporter 2 (SGLT2) inhibitors, initially developed as a novel class of anti-hyperglycaemic drugs, have been shown to significantly improve metabolic indicators and protect the kidneys and heart of patients with or without type 2 diabetes mellitus. The possible mechanisms mediating these unexpected cardiorenal benefits are being extensively investigated because they cannot solely be attributed to improvements in glycaemic control. Notably, emerging data indicate that metabolic reprogramming is involved in the progression of cardiorenal metabolic diseases. SGLT2 inhibitors reprogram systemic metabolism to a fasting-like metabolic paradigm, involving the metabolic switch from carbohydrates to other energetic substrates and regulation of the related nutrient-sensing pathways, which might explain some of their cardiorenal protective effects. In this review, we will focus on the current understanding of cardiorenal protection by SGLT2 inhibitors, specifically its relevance to metabolic reprogramming.

Correction: FADH₂ and Complex II

FADH₂ is shown as the substrate feeding electrons into Complex II (CII). This is wrong and requires correction - for details see Gnaiger (2024).

Gnaiger E (2024) Complex II ambiguities ― FADH₂ in the electron transfer system. J Biol Chem 300:105470. https://doi.org/10.1016/j.jbc.2023.105470 - »Bioblast link«

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Enzyme: Complex II;succinate dehydrogenase