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dc.contributor.author
Sanz, Raul Lelio
dc.contributor.author
García Menéndez, Sebastián Marcelo Manuel
dc.contributor.author
Inserra, Felipe
dc.contributor.author
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
dc.subject
CARDIOVASCULAR DISEASE
dc.subject.classification
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
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