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Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes?

Yurista, S., Sillje, H., Rienstra, M., Boer, de, R. & Westenbrink, D., 7-Jan-2020, In : Cardiovascular Diabetology. 19, 1, p. 5 7 p., 5.

Research output: Contribution to journal › Article › Academic › peer-review

APA

Yurista, S., Sillje, H., Rienstra, M., Boer, de, R., & Westenbrink, D. (2020). Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes? Cardiovascular Diabetology, 19(1), 5. [5]. https://doi.org/10.1186/s12933-019-0984-0

Author

Yurista, Salva ; Sillje, Herman ; Rienstra, Michiel ; Boer, de, Rudolf ; Westenbrink, Daan. / Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes?. In: Cardiovascular Diabetology. 2020 ; Vol. 19, No. 1. pp. 5.

Harvard

Yurista, S, Sillje, H, Rienstra, M, Boer, de, R & Westenbrink, D 2020, 'Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes?', Cardiovascular Diabetology, vol. 19, no. 1, 5, pp. 5. https://doi.org/10.1186/s12933-019-0984-0

Standard

Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes? / Yurista, Salva; Sillje, Herman; Rienstra, Michiel; Boer, de, Rudolf; Westenbrink, Daan.

In: Cardiovascular Diabetology, Vol. 19, No. 1, 5, 07.01.2020, p. 5.

Research output: Contribution to journal › Article › Academic › peer-review

Vancouver

Yurista S, Sillje H, Rienstra M, Boer, de R, Westenbrink D. Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes? Cardiovascular Diabetology. 2020 Jan 7;19(1):5. 5. https://doi.org/10.1186/s12933-019-0984-0

BibTeX

@article{a9fc6b901dee44188b23b2acef0007a6,
title = "Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes?",
abstract = "While patients with type 2 diabetes mellitus (T2DM) are at increased risk to develop atrial fibrillation (AF), the mechanistic link between T2DM and AF-susceptibility remains unclear. Common co-morbidities of T2DM, particularly hypertension, may drive AF in the setting of T2DM. But direct mechanisms may also explain this relation, at least in part. In this regard, recent evidence suggests that mitochondrial dysfunction drives structural, electrical and contractile remodelling of atrial tissue in patients T2DM. Mitochondrial dysfunction may therefore be the mechanistic link between T2DM and AF and could also serve as a therapeutic target. An elegant series of experiments published in Cardiovascular Diabetology provide compelling new evidence to support this hypothesis. Using a model of high fat diet (HFD) and low-dose streptozotocin (STZ) injection, Shao et al. provide data that demonstrate a direct association between mitochondrial dysfunction and the susceptibility to develop AF. But the authors also demonstrated that the sodium-glucose co-transporter 2 inhibitors (SGLT2i) empagliflozin has the capacity to restore mitochondrial function, ameliorate electrical and structural remodelling and prevent AF. These findings provide a new horizon in which mitochondrial targeted therapies could serve as a new class of antiarrhythmic drugs.",
keywords = "Mitochondria, Diabetes, Atrial fibrillation, Sodium-glucose co-transporter-2 inhibitors, RISK-FACTORS, OXIDATIVE STRESS, CAMKII, PHOSPHORYLATION, OSCILLATIONS, MYOCARDIUM, METABOLISM, MANAGEMENT, REDUCTION, MORTALITY",
author = "Salva Yurista and Herman Sillje and Michiel Rienstra and {Boer, de}, Rudolf and Daan Westenbrink",
year = "2020",
month = jan,
day = "7",
doi = "10.1186/s12933-019-0984-0",
language = "English",
volume = "19",
pages = "5",
journal = "Cardiovascular Diabetology",
issn = "1475-2840",
publisher = "BioMed Central Ltd.",
number = "1",

}

RIS

TY - JOUR

T1 - Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes?

AU - Yurista, Salva

AU - Sillje, Herman

AU - Rienstra, Michiel

AU - Boer, de, Rudolf

AU - Westenbrink, Daan

PY - 2020/1/7

Y1 - 2020/1/7

N2 - While patients with type 2 diabetes mellitus (T2DM) are at increased risk to develop atrial fibrillation (AF), the mechanistic link between T2DM and AF-susceptibility remains unclear. Common co-morbidities of T2DM, particularly hypertension, may drive AF in the setting of T2DM. But direct mechanisms may also explain this relation, at least in part. In this regard, recent evidence suggests that mitochondrial dysfunction drives structural, electrical and contractile remodelling of atrial tissue in patients T2DM. Mitochondrial dysfunction may therefore be the mechanistic link between T2DM and AF and could also serve as a therapeutic target. An elegant series of experiments published in Cardiovascular Diabetology provide compelling new evidence to support this hypothesis. Using a model of high fat diet (HFD) and low-dose streptozotocin (STZ) injection, Shao et al. provide data that demonstrate a direct association between mitochondrial dysfunction and the susceptibility to develop AF. But the authors also demonstrated that the sodium-glucose co-transporter 2 inhibitors (SGLT2i) empagliflozin has the capacity to restore mitochondrial function, ameliorate electrical and structural remodelling and prevent AF. These findings provide a new horizon in which mitochondrial targeted therapies could serve as a new class of antiarrhythmic drugs.

AB - While patients with type 2 diabetes mellitus (T2DM) are at increased risk to develop atrial fibrillation (AF), the mechanistic link between T2DM and AF-susceptibility remains unclear. Common co-morbidities of T2DM, particularly hypertension, may drive AF in the setting of T2DM. But direct mechanisms may also explain this relation, at least in part. In this regard, recent evidence suggests that mitochondrial dysfunction drives structural, electrical and contractile remodelling of atrial tissue in patients T2DM. Mitochondrial dysfunction may therefore be the mechanistic link between T2DM and AF and could also serve as a therapeutic target. An elegant series of experiments published in Cardiovascular Diabetology provide compelling new evidence to support this hypothesis. Using a model of high fat diet (HFD) and low-dose streptozotocin (STZ) injection, Shao et al. provide data that demonstrate a direct association between mitochondrial dysfunction and the susceptibility to develop AF. But the authors also demonstrated that the sodium-glucose co-transporter 2 inhibitors (SGLT2i) empagliflozin has the capacity to restore mitochondrial function, ameliorate electrical and structural remodelling and prevent AF. These findings provide a new horizon in which mitochondrial targeted therapies could serve as a new class of antiarrhythmic drugs.

KW - Mitochondria

KW - Diabetes

KW - Atrial fibrillation

KW - Sodium-glucose co-transporter-2 inhibitors

KW - RISK-FACTORS

KW - OXIDATIVE STRESS

KW - CAMKII

KW - PHOSPHORYLATION

KW - OSCILLATIONS

KW - MYOCARDIUM

KW - METABOLISM

KW - MANAGEMENT

KW - REDUCTION

KW - MORTALITY

U2 - 10.1186/s12933-019-0984-0

DO - 10.1186/s12933-019-0984-0

M3 - Article

C2 - 31910841

VL - 19

SP - 5

JO - Cardiovascular Diabetology

JF - Cardiovascular Diabetology

SN - 1475-2840

IS - 1

M1 - 5

ER -

ID: 118188480

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