Results 41 to 50 of about 20,923 (159)

The sodium–glucose co-transporter 2 inhibitor empagliflozin attenuates cardiac fibrosis and improves ventricular hemodynamics in hypertensive heart failure rats

open access: yesCardiovascular Diabetology, 2019
Background Sodium glucose co-transporter 2 inhibitor (SGLT2i), a new class of anti-diabetic drugs acting on inhibiting glucose resorption by kidneys, is shown beneficial in reduction of heart failure hospitalization and cardiovascular mortality.
Hsiang-Chun Lee   +9 more
doaj   +1 more source

Empagliflozin attenuates cardiac microvascular ischemia/reperfusion through activating the AMPKα1/ULK1/FUNDC1/mitophagy pathway

open access: yesRedox Biology, 2022
Mitophagy preserves microvascular structure and function during myocardial ischemia/reperfusion (I/R) injury. Empagliflozin, an anti-diabetes drug, may also protect mitochondria.
Chen Cai   +12 more
doaj   +1 more source

Empagliflozin Suppresses the Differentiation/Maturation of Human Epicardial Preadipocytes and Improves Paracrine Secretome Profile

open access: yesJACC: Basic to Translational Science, 2023
Summary: Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce epicardial adipose tissue (EAT) in humans, enhancing cardioprotective effects on heart failure and atrial fibrillation.
Masayuki Takano, MD   +15 more
doaj   +1 more source

Empagliflozin Ameliorates Experimental Pulmonary Vascular Remodeling, but May Not Benefit Patients With Pulmonary Arterial Hypertension

open access: yesJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Background Sodium glucose cotransporter 2 inhibitors may improve mitochondrial biogenesis and attenuate pulmonary vascular remodeling in pulmonary arterial hypertension (PAH). We investigated the impact of empagliflozin in PAH.
Keimei Yoshida   +13 more
doaj   +1 more source

Decoding empagliflozin’s molecular mechanism of action in heart failure with preserved ejection fraction using artificial intelligence

open access: yesScientific Reports, 2021
The use of sodium-glucose co-transporter 2 inhibitors to treat heart failure with preserved ejection fraction (HFpEF) is under investigation in ongoing clinical trials, but the exact mechanism of action is unclear.
Antoni Bayes-Genis   +11 more
doaj   +1 more source

Comparison of Adverse Kidney Outcomes With Empagliflozin and Linagliptin Use in Patients With Type 2 Diabetic Patients in a Real-World Setting

open access: yesFrontiers in Pharmacology, 2021
Background: To compare the effects of empagliflozin and linagliptin use on kidney outcomes of type 2 diabetes mellitus (T2DM) patients in a real-world setting.Methods: The study involved a propensity score-matched cohort comprising new users of ...
Yueh-Ting Lee   +7 more
doaj   +1 more source

Empagliflozin after acute myocardial infarction. [PDF]

open access: yes
BACKGROUND Empagliflozin improves cardiovascular outcomes in patients with heart failure, patients with type 2 diabetes who are at high cardiovascular risk, and patients with chronic kidney disease.
Figtree, Gemma   +81 more
core   +1 more source

Empagliflozin for treating neutropenia and neutrophil dysfunction in 21 infants with glycogen storage disease 1b. [PDF]

open access: yes
Empagliflozin has been successfully repurposed for treating neutropenia and neutrophil dysfunction in patients with glycogen storage disease type 1b (GSD 1b), however, data in infants are missing.
Boyer, M.   +58 more
core   +2 more sources

Supplemental figures for Reno-protective Effects of Empagliflozin

open access: yes, 2023
The mechanisms of nephroprotection in non-diabetic chronic kidney disease (CKD) models by sodium-glucose cotransporter 2 (SGLT2) inhibitors are not well defined. Five groups were established: sham operated rats, placebo treated rats with 5/6 nephrectomy (
Hongwei Wu (1234719)   +15 more
core   +1 more source

Empagliflozin significantly attenuates sotalol-induced QTc prolongation in rats [PDF]

open access: yes, 2021
Background: Sotalol is a class III antiarrhythmic drug commonly used in various arrhythmia treatments. However, due to its potent potassium channel inhibition, it can prolong the QT interval and lead to malignant arrhythmias.
Dinçsoy, Berk   +7 more
core   +2 more sources

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