Evidence map›Paper›PMID 37391739›Full record

ReviewCardiovascular diabetology2023

Pathophysiological basis of the cardiological benefits of SGLT-2 inhibitors: a narrative review.

Cristina Panico, Benedetta Bonora, Antonella Camera, Nino Cristiano Chilelli, Giuliana Da Prato, Giuseppe Favacchio, Valeria Grancini, Veronica Resi, Maurizio Rondinelli, Emanuela Zarra and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Cardiovascular diabetology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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  12. Glucagon-like peptide-1 receptor: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024 · on this map
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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

11 authors at 8 institutions in 1 country.

Cristina PanicoDepartment of Biomedical Sciences, Humanitas University, Pieve Emanuele-Milan, Italy. cristina.panico@hunimed.eu.
Benedetta BonoraDepartment of Medicine, Division of Metabolic Diseases, University of Padova, Via Giustiniani 2, Padua, 35128, Italy.
Antonella CameraDiabetologia, ASST Pavia, Padua, Italy.
Nino Cristiano ChilelliDiabetology and Internal Medicine, Hospital of Cittadella, AULSS 6 Euganea (Padua), Padua, Italy.
Giuliana Da PratoDivisione di Endocrinologia, Diabetologia e Malattie del Metabolismo, Dipartimento di Medicina, Azienda Ospedaliera Universitaria Integrata di Verona, Ospedale Maggiore, Verona, Italy.
Giuseppe FavacchioU.O di Endocrinologia e Diabetologia, IRCCS Humanitas Research Hospital, Rozzano, MI, Italy.
Valeria GranciniEndocrinology Unit, Fondazione IRCCS Ca' Granda - Ospedale Maggiore Policlinico, Milan, Italy.
Veronica ResiEndocrinology Unit, Fondazione IRCCS Ca' Granda - Ospedale Maggiore Policlinico, Milan, Italy.
Maurizio RondinelliDiabetes Endocrine and Metabolic Diseases Unit, IRCCS Centro Cardiologico Monzino, Milan, Italy.
Emanuela ZarraS.C. Medicina Diabetologia, Dipartimento di Continuità di Cura e Fragilità, ASST Spedali Civili, Brescia, Italy.
Basilio PintaudiDiabetes Unit, Niguarda Hospital, Milan, Italy.
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITAzienda Socio Sanitaria Territoriale degli Spedali Civili di Brescia · ITAzienda Socio Sanitaria Territoriale Grande Ospedale Metropolitano Niguarda · ITCentro Cardiologico Monzino · ITHumanitas University · ITIRCCS Humanitas Research Hospital · ITOspedale Maggiore · ITUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years, GLP-1 receptor agonists (GLP-1RA), and SGLT-2 inhibitors (SGLT-2i) have become available, which have become valuable additions to therapy for type 2 diabetes as they are associated with low risk for hypoglycemia and cardiovascular benefits. Indeed, SGLT-2i have emerged as a promising class of agents to treat heart failure (HF). By inhibiting SGLT-2, these agents lead to excretion of glucose in urine with subsequent lowering of plasma glucose, although it is becoming clear that the observed benefits in HF cannot be explained by glucose-lowering alone. In fact, multiple mechanisms have been proposed to explain the cardiovascular and renal benefits of SGLT-2i, including hemodynamic, anti-inflammatory, anti-fibrotic, antioxidant, and metabolic effects. Herein, we review the available evidence on the pathophysiology of the cardiological benefits of SGLT-2i. In diabetic heart disease, in both clinical and animal models, the effect of SGLT-2i have been shown to improve diastolic function, which is even more evident in HF with preserved ejection fraction. The probable pathogenic mechanisms likely involve damage from free radicals, apoptosis, and inflammation, and therefore fibrosis, many of which have been shown to be improved by SGLT-2i. While the effects on systolic function in models of diabetic heart disease and HF with preserved ejection fraction is limited and contrasting, it is a key element in patients with HF and reduced ejection fraction both with and without diabetes. The significant improvement in systolic function appears to lead to subsequent structural remodeling of the heart with a reduction in left ventricle volume and a consequent reduction in pulmonary pressure. While the effects on cardiac metabolism and inflammation appear to be consolidated, greater efforts are still warranted to further define the entity to which these mechanisms contribute to the cardiovascular benefits of SGLT-2i.

Indexed as

Diabetes Mellitus, Type 2Heart FailureSodium-Glucose Transporter 2 InhibitorsAnimalsGlucoseHeart VentriclesInflammationGlucoseSodium-Glucose Transporter 2 InhibitorsCardiovascularHeart failureMechanism of actionPathophysiologySGLT2 inhibitorsType 2 diabetes

Identifiers

PMID37391739
PMCPMC10314539
OpenAlexW4382776744

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.