Empagliflozin Significantly Prevents the Doxorubicin-induced Acute Cardiotoxicity via Non-antioxidant Pathways

Barış, Veysel Özgür; Dinçsoy, Adnan Berk; Gedikli, Esra; Zırh, Selim; Müftüoğlu, Sevda; Erdem, Ayşen

doi:10.1007/s12012-021-09665-y

Cited by 29 publications

(22 citation statements)

References 58 publications

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“…NF-kB and the NLRP3 inflammasome by 25-40%, as well as downregulation of the mTORC mediated pathway to apoptosis. In a rodent model, empagliflozin with doxorubicin administration led to preservation of LVEF and longitudinal strain with histologic evidence of reduced myocardial fibrosis and apoptosis (34)(35)(36).…”

Section: Sodium-glucose Transport Protein 2 Inhibitorsmentioning

confidence: 98%

Novel Therapeutics for Anthracycline Induced Cardiotoxicity

Vuong

Stein-Merlob

Cheng

et al. 2022

Front. Cardiovasc. Med.

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Anthracyclines remain an essential component of the treatment of many hematologic and solid organ malignancies, but has important implications on cardiovascular disease. Anthracycline induced cardiotoxicity (AIC) ranges from asymptomatic LV dysfunction to highly morbid end- stage heart failure. As cancer survivorship improves, the detection and treatment of AIC becomes more crucial to improve patient outcomes. Current treatment modalities for AIC have been largely extrapolated from treatment of conventional heart failure, but developing effective therapies specific to AIC is an area of growing research interest. This review summarizes the current evidence behind the use of neurohormonal agents, dexrazoxane, and resynchronization therapy in AIC, evaluates the clinical outcomes of advanced therapy and heart transplantation in AIC, and explores future horizons for treatment utilizing gene therapy, stem cell therapy, and mechanism-specific targets.

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Section: Sodium-glucose Transport Protein 2 Inhibitorsmentioning

confidence: 98%

Novel Therapeutics for Anthracycline Induced Cardiotoxicity

Vuong

Stein-Merlob

Cheng

et al. 2022

Front. Cardiovasc. Med.

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“…Subsequent to landmark studies demonstrating the cardioprotective effects of SGLT2 inhibitors in HF, numerous in vivo ( Table 2 ) and in vitro ( Table 3 ) studies, starting in 2019, have underscored the cardioprotective roles of SGLT2 inhibitors in mitigating cardiotoxicity induced by various cancer treatments, including DOX, 17 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 sunitinib, 20 trastuzumab, 21 cisplatin, 19 ipilmumab, 54 , 55 ponatinib, 56 and carfilzomib. 57 DOX has received particular attention because of its status as the most cardiotoxic cancer treatment and its widespread use.…”

Section: Sglt2 Inhibitors In Cardio-oncologymentioning

confidence: 99%

The Cardioprotective and Anticancer Effects of SGLT2 Inhibitors

Dabour,

George,

Daniel

et al. 2024

JACC: CardioOncology

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“…Recently, the potentially protective effects of SGLT2 inhibitors on the cardiac dysfunction induced by chemotherapies and targeted therapies were also investigated in preclinical studies in animal models. In this regard, protective effect by empagliflozin against anthracycline-induced cardiac impairment, diastolic dysfunction, and maladaptive cardiac remodeling has been documented (256)(257)(258)(259). Mechanistically, empagliflozin was suggested to reduce ferroptosis, inflammatory response (NF-κB signaling), apoptosis, and fibrosis induced by doxorubicin through the involvement of NLRP3 and MyD88-related pathway (257,258).…”

Section: Sodium-glucose Cotransporter-2 Inhibitorsmentioning

confidence: 99%

Cardiotoxicity of Anticancer Drugs: Molecular Mechanisms and Strategies for Cardioprotection

Morelli

Bongiovanni

Pra

et al. 2022

Front. Cardiovasc. Med.

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Chemotherapy and targeted therapies have significantly improved the prognosis of oncology patients. However, these antineoplastic treatments may also induce adverse cardiovascular effects, which may lead to acute or delayed onset of cardiac dysfunction. These common cardiovascular complications, commonly referred to as cardiotoxicity, not only may require the modification, suspension, or withdrawal of life-saving antineoplastic therapies, with the risk of reducing their efficacy, but can also strongly impact the quality of life and overall survival, regardless of the oncological prognosis. The onset of cardiotoxicity may depend on the class, dose, route, and duration of administration of anticancer drugs, as well as on individual risk factors. Importantly, the cardiotoxic side effects may be reversible, if cardiac function is restored upon discontinuation of the therapy, or irreversible, characterized by injury and loss of cardiac muscle cells. Subclinical myocardial dysfunction induced by anticancer therapies may also subsequently evolve in symptomatic congestive heart failure. Hence, there is an urgent need for cardioprotective therapies to reduce the clinical and subclinical cardiotoxicity onset and progression and to limit the acute or chronic manifestation of cardiac damages. In this review, we summarize the knowledge regarding the cellular and molecular mechanisms contributing to the onset of cardiotoxicity associated with common classes of chemotherapy and targeted therapy drugs. Furthermore, we describe and discuss current and potential strategies to cope with the cardiotoxic side effects as well as cardioprotective preventive approaches that may be useful to flank anticancer therapies.

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Empagliflozin Significantly Prevents the Doxorubicin-induced Acute Cardiotoxicity via Non-antioxidant Pathways

Cited by 29 publications

References 58 publications

Novel Therapeutics for Anthracycline Induced Cardiotoxicity

Novel Therapeutics for Anthracycline Induced Cardiotoxicity

The Cardioprotective and Anticancer Effects of SGLT2 Inhibitors

Cardiotoxicity of Anticancer Drugs: Molecular Mechanisms and Strategies for Cardioprotection

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