MCAD activation by empagliflozin promotes fatty acid oxidation and reduces lipid deposition in NASH - PubMed
Source : https://pubmed.ncbi.nlm.nih.gov/35900373/
Medium chain acyl-CoA dehydrogenase (MCAD) is one of the significant enzymes involved in β-oxidation of mitochondrial fatty acids. MCAD deficiency affects the β-oxidation of fatty acid and leads to lipid...
Conclusion/Relevance: Empagliflozin could upregulate MCAD expression by activating AMPK/FOXA2 signaling pathway, reduce lipid deposition and improve NASH in vivo and in vitro. This research demonstrated that MCAD is a key player of hepatic lipid deposition and it's targeting partially corrects NASH. MCAD thus may be a potential therapeutic...
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Differential In Vitro Effects of SGLT2 Inhibitors on Mitochondrial Oxidative Phosphorylation, Glucose Uptake and Cell Metabolism - PubMed
Source : https://pubmed.ncbi.nlm.nih.gov/35887308/
1 Institute for Biomedicine and Health Sciences (HEALTH), Joanneum Research Forschungsgesellschaft m.b.H, Neue Stiftingtalstrasse 2, 8010 Graz, Austria. 2 Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca,...
Relevance: The cardio-reno-metabolic benefits of the SGLT2 inhibitors canagliflozin (cana), dapagliflozin (dapa), ertugliflozin (ertu), and empagliflozin (empa) have been demonstrated, but it remains unclear whether they exert different off-target effects influencing clinical profiles. We aimed to investigate the effects of SGLT2 inhibitors...
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Resting Cardiac Power Predicts Adverse Outcome in Heart Failure Patients With Preserved Ejection Fraction: A Prospective Study
Source : https://www.frontiersin.org/articles/10.3389/fcvm.2022.915918/full
BackgroundWe sought to explore the significance of resting cardiac power/mass in predicting adverse outcome in patients with heart failure with preserved ejection fraction (HFpEF).MethodsThis prospective cohort study included patients with...
Conclusion: Resting cardiac power determined by non-invasive echocardiography is independently associated with the risk of adverse outcomes in HFpEF patients and provides incremental prognostic information.
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Empagliflozin activates Wnt/β-catenin to stimulate FUNDC1-dependent mitochondrial quality surveillance against type-3 cardiorenal syndrome
Source : https://www.sciencedirect.com/science/article/pii/S2212877822001223?via=ihub
Empagliflozin reduces myocardial damage and improves myocardial function after CRS-3. * Empagliflozin normalizes the mitochondrial structure in cardiomyocytes during CRS-3. * Empagliflozin attenuates cardiomyocyte mitochondrial dysfunction during CRS-3. * Empagliflozin...
Conclusion: In summary, empagliflozin activated Wnt/β-catenin to stimulate FUNDC1-dependent mitochondrial quality surveillance, ultimately improving mitochondrial function and cardiac performance during CRS-3. Thus, empagliflozin could be considered for the clinical management of heart function following acute kidney injury.
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Sodium-Glucose Cotransporter 2 Inhibitors in Heart Failure with Preserved Ejection Fraction: Rationale for and Practical Use of a Successful Therapy
Until 2021, medical treatment of patients with heart failure (HF) and preserved ejection fraction (HFpEF) was mainly limited to diuretics to improve symptoms of HF, while no therapies demonstrated a...
Conclusion: The authors describe the rationale for this therapy, presenting the main results of the EMPEROR-Preserved trial, and provide some recommendations for the everyday clinical management of HF with preserved left ventricular ejection with an SGLT2I.
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