Dapagliflozin and DAPA‐HF: from glycaemic control to heart failure therapy

Fisher, Miles

doi:10.1002/pdi.2243

Cited by 2 publications

(2 citation statements)

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“…Additionally, existing studies have pointed out that glucose and lipid metabolism disorders caused by hyperglycemia will trigger an increase in oxidative stress in the body, resulting in mitochondrial dysfunction in cardiomyocytes and dynamic imbalance of calcium, which eventually induces cardiac dysfunction. Fortunately, DAPA can reduce blood glucose content by increasing glucose excretion in T2DM and alleviate cardiac dysfunction caused by hyperglycemia [ 20 , 21 ].…”

Section: Discussionmentioning

confidence: 99%

Dapagliflozin Ameliorates STZ-Induced Cardiac Hypertrophy in Type 2 Diabetic Rats by Inhibiting the Calpain-1 Expression and Nuclear Transfer of NF-κB

Liu

Luo

Liang

et al. 2022

Computational and Mathematical Methods in Medicine

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Objective. To investigate the effect of dapagliflozin (DAPA) on cardiac hypertrophy induced by type 2 diabetes mellitus (T2DM) and its mechanism. Methods. SD rats with T2DM were divided into a T2DM group ( n = 6 ) and DAPA group ( n = 6 ). They were, respectively, fed with the same amount of normal saline and 1 mg/kg DAPA. The control group ( n = 6 ) was also fed with normal saline. The hearts were tested by the application of echocardiography and hemodynamics. Subsequently, fasting blood glucose (FBG), serum total cholesterol (TC), and triglyceride (TG) as well as interleukin- (IL-) 10, IL-6, and tumor necrosis factor (TNF)-α in serum were tested. H&E and Masson staining was performed to observe the degree of cardiac tissue lesions, and expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), calpain-1, p-IκBα, and p65 in myocardial tissue was tested by qRT-PCR and Western blot. Results. Compared with the control group, rats in the T2DM group exhibited significant diabetic symptoms: FBG was significantly elevated, and the levels of TC, TG, IL-6, and TNF-α were significantly increased, while the levels of IL-10 and the calpain activity were evidently decreased. However, DAPA treatment could improve the above changes. At the same time, the damage and fibrosis of the heart tissue in the DAPA group were markedly improved. Additionally, the mRNA expression of ANP and BNP in myocardial tissue of the DAPA group was markedly increased. And DAPA could inhibit the expression of p-IκBα/IκBα in the cytoplasm and p65 in the nucleus as well as the expression of calpain-1 in myocardial tissue. Conclusion. DAPA treatment ameliorates the cardiac hypertrophy caused by T2DM by decreasing body blood glucose, while reducing the expression of calpain-1 in cardiomyocytes and inhibiting the nuclear translocation of NF-κB.

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Section: Discussionmentioning

confidence: 99%

Dapagliflozin Ameliorates STZ-Induced Cardiac Hypertrophy in Type 2 Diabetic Rats by Inhibiting the Calpain-1 Expression and Nuclear Transfer of NF-κB

Liu

Luo

Liang

et al. 2022

Computational and Mathematical Methods in Medicine

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“…Before commencing therapy the primary care physician should consider any factors within the patient's history that would predispose to ketoacidosis. Awareness of possible volume depletion during intercurrent illness is important, with strict adherence to ‘sick day rules’ 7 …”

Section: Use In Clinical Practicementioning

confidence: 99%

Dapagliflozin for heart failure

Begg

2021

Practical Diabetes

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Dapagliflozin and DAPA‐HF: from glycaemic control to heart failure therapy

Cited by 2 publications

References 13 publications

Dapagliflozin Ameliorates STZ-Induced Cardiac Hypertrophy in Type 2 Diabetic Rats by Inhibiting the Calpain-1 Expression and Nuclear Transfer of NF-κB

Dapagliflozin Ameliorates STZ-Induced Cardiac Hypertrophy in Type 2 Diabetic Rats by Inhibiting the Calpain-1 Expression and Nuclear Transfer of NF-κB

Dapagliflozin for heart failure

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