Sodium–glucose cotransporter 2 inhibitors and the cancer patient: from diabetes to cardioprotection and beyond

Camilli, Massimiliano ✉; Viscovo, Marcello*; Maggio, Luca*; Bonanni, Alice; Torre, Ilaria; Pellegrino, Claudio; Lamendola, Priscilla; Tinti, Lorenzo; Teofili, Luciana; Hohaus, Stefan; Lanza, Gaetano Antonio; Ferdinandy, Peter [Ferdinandy, Péter (Farmakológia, mol...), szerző] Farmakológiai és Farmakoterápiás Intézet (SE / AOK / I); MTA-SE Rendszerfarmakológiai Kutatócsoport (SE / AOK / I / FFI); Varga, Zoltan [Varga, Zoltán (kardiovaszkuláris...), szerző] Farmakológiai és Farmakoterápiás Intézet (SE / AOK / I); HCEMM-SE Kardiometabolikus Immunológia Kutatócs... (SE / AOK / I / FFI); MTA-SE Momentum Kardio-Onkológia és Kardioimmun... (SE / AOK / I / FFI); Crea, Filippo; Lombardo, Antonella; Minotti, Giorgio

Angol nyelvű Összefoglaló cikk (Folyóiratcikk) Tudományos
Megjelent: BASIC RESEARCH IN CARDIOLOGY 0300-8428 1435-1803 120 pp. 241-262 2025
  • SJR Scopus - Cardiology and Cardiovascular Medicine: D1
Azonosítók
Sodium–glucose cotransporter 2 inhibitors (SGLT2i), a new drug class initially designed and approved for treatment of diabetes mellitus, have been shown to exert pleiotropic metabolic and direct cardioprotective and nephroprotective effects that extend beyond their glucose-lowering action. These properties prompted their use in two frequently intertwined conditions, heart failure and chronic kidney disease. Their unique mechanism of action makes SGLT2i an attractive option also to lower the rate of cardiac events and improve overall survival of oncological patients with preexisting cardiovascular risk and/or candidate to receive cardiotoxic therapies. This review will cover biological foundations and clinical evidence for SGLT2i modulating myocardial function and metabolism, with a focus on their possible use as cardioprotective agents in the cardio-oncology settings. Furthermore, we will explore recently emerged SGLT2i effects on hematopoiesis and immune system, carrying the potential of attenuating tumor growth and chemotherapy-induced cytopenias.
Hivatkozás stílusok: IEEEACMAPAChicagoHarvardCSLMásolásNyomtatás
2025-04-03 11:00