SynthesisEuropean journal of heart failure2025
Unlocking the power of empagliflozin: Rescuing inflammation in hyperglycaemia-exposed human cardiomyocytes through comprehensive multi-level analysis.
Synthesis in European journal of heart failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
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Who cites it
3 citing papers in PubMed.
- Effects of Vericiguat on the Mitochondrial Function and Clinical Outcomes in CRT Nonresponders Patients.JACC. Advances · 2026Article
- CauReL: Dynamic Counterfactual Learning for Precision Drug Repurposing in Alzheimer's Disease.Research square · 2025Article
- Heart failure: mechanistic insights and precision therapeutic strategies.Frontiers in cardiovascular medicine · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
aimsHyperglycaemic conditions increase cardiac stress, a common phenomenon associated with inflammation, aging, and metabolic imbalance. Sodium-glucose cotransporter 2 inhibitors, a class of anti-diabetic drugs, showed to improve cardiovascular functions although their mechanism of action has not yet been fully established. This study investigated the effects of empagliflozin on cardiomyocytes following high glucose exposure, specifically focusing on inflammatory and metabolic responses. METHODS AND
resultsA three-part strategy was formulated: (i) a meta-analysis of selected randomized clinical trials was carried out to assess the anti-inflammatory effects of empagliflozin in diabetic patients; (ii) the impact of empagliflozin on human cardiomyocyte AC16 cells exposed to normal (5 mM) and high (33 mM) glucose concentrations for 2 and 7 days was explored by evaluating gene expression and protein levels of pivotal markers associated with cardiac inflammation, stress, endoplasmic reticulum damage, and calcium modulation; (iii) in silico data from bioinformatic analyses were exploited to construct an interaction map delineating the potential mechanism of action of empagliflozin on cardiac tissue. Empagliflozin reversed high-glucose mediated alterations at the transcriptional level, decreasing inflammatory, metabolic, and aging signatures. Specifically, in vitro experiments on human cardiomyocytes, meta-analyses of clinical data on inflammatory biomarkers from diabetic peripheral blood samples, and sequencing of pathological human heart tissues, all support that empagliflozin exerts anti-inflammatory effects both systemically and directly in cardiac tissue, on cardiomyocytes.
conclusionOur study provides insights based on robust mechanistic data for optimizing heart failure management and highlights the intricate interplay between diabetes, inflammation, aging, and cardiovascular health.
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Registered trials
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.