Evidence map›Paper›PMID 38551044›Full record

ReviewCurrent pharmaceutical design2024

Cellular and Mitochondrial Pathways Contribute to SGLT2 Inhibitors-mediated Tissue Protection: Experimental and Clinical Data.

Raúl Lelio Sanz, Sebastián García Menéndez, Felipe Inserra, León Ferder, Walter Manucha

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current pharmaceutical design, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 10 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Raúl Lelio SanzDepartamento de Patologie et Pharmacologie, Instituto de Medicina y Biologia Experimental de Cuyo, Consejo Nacional de Investigación Cientifica y Tecnológica (IMBECU- CONICET), Mendoza 5500, Argentina.
Sebastián García MenéndezDepartamento de Patologie et Pharmacologie, Instituto de Medicina y Biologia Experimental de Cuyo, Consejo Nacional de Investigación Cientifica y Tecnológica (IMBECU- CONICET), Mendoza 5500, Argentina.
Felipe InserraDepartmento de Pathologie et Pharmacologie, Universidad Maimónides, Buenos Aires C1405, Argentina.
León FerderDepartmento de Pathologie et Pharmacologie, Universidad Maimónides, Buenos Aires C1405, Argentina.
Walter ManuchaDepartamento de Patologie et Pharmacologie, Instituto de Medicina y Biologia Experimental de Cuyo, Consejo Nacional de Investigación Cientifica y Tecnológica (IMBECU- CONICET), Mendoza 5500, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARUniversidad Maimónides · ARInstituto de Medicina y Biología Experimental de Cuyo · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

MitochondriaSodium-Glucose Transporter 2 InhibitorsAnimalsCardiovascular DiseasesHumansSodium-Glucose Transporter 2 Inhibitorscardiovascular diseasesinflammationmitochondrial dysfunction.oxidative stressSGLT2isirtuins

Identifiers

PMID38551044
OpenAlexW4393312745

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.