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dc.contributor.author
Sanz, Raul Lelio  
dc.contributor.author
García Menéndez, Sebastián Marcelo Manuel  
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Inserra, Felipe  
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Ferder, León  
dc.contributor.author
Manucha, Walter Ariel Fernando  
dc.date.available
2025-04-25T09:07:01Z  
dc.date.issued
2024-03  
dc.identifier.citation
Sanz, Raul Lelio; García Menéndez, Sebastián Marcelo Manuel; Inserra, Felipe; Ferder, León; Manucha, Walter Ariel Fernando; Cellular and Mitochondrial Pathways Contribute to SGLT2 Inhibitors-mediated Tissue Protection: Experimental and Clinical Data; Bentham Science Publishers; Current Pharmaceutical Design; 30; 13; 3-2024; 969-974  
dc.identifier.issn
1381-6128  
dc.identifier.uri
http://hdl.handle.net/11336/259555  
dc.description.abstract
In metabolic syndrome and diabetes, compromised mitochondrial function emerges as a critical driver of cardiovascular disease, fueling its development and persistence, culminating in cardiac remodeling and adverse events. In this context, angiotensin II - the main interlocutor of the renin-angiotensin-aldosterone system - promotes local and systemic oxidative inflammatory processes. To highlight, the low activity/expression of proteins called sirtuins negatively participates in these processes, allowing more significant oxidative imbalance, which impacts cellular and tissue responses, causing tissue damage, inflammation, and cardiac and vascular remodeling. The reduction in energy production of mitochondria has been widely described as a significant element in all types of metabolic disorders. Additionally, high sirtuin levels and AMPK signaling stimulate hypoxia-inducible factor 1 beta and promote ketonemia. Consequently, enhanced autophagy and mitophagy advance through cardiac cells, sweeping away debris and silencing the orchestra of oxidative stress and inflammation, ultimately protecting vulnerable tissue from damage. To highlight and of particular interest, SGLT2 inhibitors (SGLT2i) profoundly influence all these mechanisms. Randomized clinical trials have evidenced a compelling picture of SGLT2i emerging as game-changers, wielding their power to demonstrably improve cardiac function and slash the rates of cardiovascular and renal events. Furthermore, driven by recent evidence, SGLT2i emerge as cellular supermolecules, exerting their beneficial actions to increase mitochondrial efficiency, alleviate oxidative stress, and curb severe inflammation. Its actions strengthen tissues and create a resilient defense against disease. In conclusion, like a treasure chest brimming with untold riches, the influence of SGLT2i on mitochondrial function holds untold potential for cardiovascular health. Unlocking these secrets, like a map guiding adventurers to hidden riches, promises to pave the way for even more potent therapeutic strategies.  
dc.format
application/pdf  
dc.language.iso
eng  
dc.publisher
Bentham Science Publishers  
dc.rights
info:eu-repo/semantics/restrictedAccess  
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/  
dc.subject
SIRTUINS  
dc.subject
SGLT2i  
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MITOCHONDRIAL  
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CARDIOVASCULAR DISEASE  
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Farmacología y Farmacia  
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Medicina Básica  
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CIENCIAS MÉDICAS Y DE LA SALUD  
dc.title
Cellular and Mitochondrial Pathways Contribute to SGLT2 Inhibitors-mediated Tissue Protection: Experimental and Clinical Data  
dc.type
info:eu-repo/semantics/article  
dc.type
info:ar-repo/semantics/artículo  
dc.type
info:eu-repo/semantics/publishedVersion  
dc.date.updated
2025-04-24T09:49:32Z  
dc.journal.volume
30  
dc.journal.number
13  
dc.journal.pagination
969-974  
dc.journal.pais
Estados Unidos  
dc.journal.ciudad
Oak Park  
dc.description.fil
Fil: Sanz, Raul Lelio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina  
dc.description.fil
Fil: García Menéndez, Sebastián Marcelo Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina  
dc.description.fil
Fil: Inserra, Felipe. Universidad Maimónides; Argentina  
dc.description.fil
Fil: Ferder, León. Universidad Maimónides; Argentina  
dc.description.fil
Fil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina  
dc.journal.title
Current Pharmaceutical Design  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.2174/0113816128289350240320063045