Evidence mapPaperPMID 38424560Full record

ArticleCardiovascular diabetology2024

The SGLT2 inhibitor Empagliflozin promotes post-stroke functional recovery in diabetic mice.

Ellen Vercalsteren, Dimitra Karampatsi, Carolina Buizza, Thomas Nyström, Thomas Klein, Gesine Paul, Cesare Patrone, Vladimer Darsalia

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

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  7. Sodium-glucose cotransporter 2 inhibitors and atherosclerosis.American journal of preventive cardiology · 2025
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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

8 authors at 3 institutions in 2 countries.

Ellen VercalsterenNeuroCardioMetabol Group, Department of Clinical Science and Education, Södersjukhuset, Internal Medicine, Karolinska Institutet, 118 83, Stockholm, Sweden. ellen.vercalsteren@ki.se.ORCID 0000-0002-9425-4209
Dimitra KarampatsiNeuroCardioMetabol Group, Department of Clinical Science and Education, Södersjukhuset, Internal Medicine, Karolinska Institutet, 118 83, Stockholm, Sweden.
Carolina BuizzaTranslational Neurology Group, Department of Clinical Science, Wallenberg Neuroscience Center and Wallenberg Center for Molecular Medicine, Lund University, Lund, Sweden.
Thomas NyströmNeuroCardioMetabol Group, Department of Clinical Science and Education, Södersjukhuset, Internal Medicine, Karolinska Institutet, 118 83, Stockholm, Sweden.
Thomas KleinBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach, Germany.
Gesine PaulTranslational Neurology Group, Department of Clinical Science, Wallenberg Neuroscience Center and Wallenberg Center for Molecular Medicine, Lund University, Lund, Sweden.
Cesare PatroneNeuroCardioMetabol Group, Department of Clinical Science and Education, Södersjukhuset, Internal Medicine, Karolinska Institutet, 118 83, Stockholm, Sweden. cesare.patrone@ki.se.ORCID 0000-0003-0470-4606
Vladimer DarsaliaNeuroCardioMetabol Group, Department of Clinical Science and Education, Södersjukhuset, Internal Medicine, Karolinska Institutet, 118 83, Stockholm, Sweden. vladimer.darsalia@ki.se.ORCID 0000-0002-6693-934X
Karolinska Institutet · SELund University · SEBoehringer Ingelheim (Germany) · DE

Funding

ALF Stockholm 951953Foundation for Geriatric Diseases at Karolinska Institutet 2022-01273Swedish Medical Research Council 2022-00577
6 · The paper itself

Abstract

Type-2 diabetes (T2D) worsens stroke recovery, amplifying post-stroke disabilities. Currently, there are no therapies targeting this important clinical problem. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are potent anti-diabetic drugs that also efficiently reduce cardiovascular death and heart failure. In addition, SGLT2i facilitate several processes implicated in stroke recovery. However, the potential efficacy of SGLT2i to improve stroke recovery in T2D has not been investigated. Therefore, we determined whether a post-stroke intervention with the SGLT2i Empagliflozin could improve stroke recovery in T2D mice. T2D was induced in C57BL6J mice by 8 months of high-fat diet feeding. Hereafter, animals were subjected to transient middle cerebral artery occlusion and treated with vehicle or the SGLTi Empagliflozin (10 mg/kg/day) starting from 3 days after stroke. A similar study in non diabetic mice was also conducted. Stroke recovery was assessed using the forepaw grip strength test. To identify potential mechanisms involved in the Empagliflozin-mediated effects, several metabolic parameters were assessed. Additionally, neuronal survival, neuroinflammation, neurogenesis and cerebral vascularization were analyzed using immunohistochemistry/quantitative microscopy. Empagliflozin significantly improved stroke recovery in T2D but not in non-diabetic mice. Improvement of functional recovery was associated with lowered glycemia, increased serum levels of fibroblast growth factor-21 (FGF-21), and the normalization of T2D-induced aberration of parenchymal pericyte density. The global T2D-epidemic and the fact that T2D is a major risk factor for stroke are drastically increasing the number of people in need of efficacious therapies to improve stroke recovery. Our data provide a strong incentive for the potential use of SGLT2i for the treatment of post-stroke sequelae in T2D.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Sodium-Glucose Transporter 2 InhibitorsAnimalsBenzhydryl CompoundsGlucosidesHumansMiceBenzhydryl CompoundsempagliflozinGlucosidesSodium-Glucose Transporter 2 InhibitorsDiabetesEmpagliflozinMouseSodium-glucose cotransporter 2 inhibitorsStroke recovery

Identifiers

PMID38424560
PMCPMC10905950
OpenAlexW4392298294

What Socratic 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 Socratic graph.