ReviewNature reviews. Cardiology2023
SGLT2 inhibitors: role in protective reprogramming of cardiac nutrient transport and metabolism.
Review in Nature reviews. Cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
113 citing papers in PubMed, 2 syntheses or guidelines pooled it, 152 citations in OpenAlex.
- SGLT2 inhibitors are associated with reductions in epicardial adipose tissue volume and thickness: a meta-analysis.International journal of obesity (2005) · 2026Pooled it
- Selective sodium-glucose cotransporter-2 inhibitors in the improvement of hemoglobin and hematocrit in patients with type 2 diabetes mellitus: a network meta-analysis.Frontiers in endocrinology · 2024Pooled it
- Empagliflozin in STEMI Patients: A Randomized Controlled Trial on Left Ventricular Recovery and Cardiovascular Outcomes.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2026Trial
- Effects of Zibotentan Alone and in Combination with Dapagliflozin on Fluid Retention in Patients with CKD.Journal of the American Society of Nephrology : JASN · 2024Trial
- Metabolic and Lipoprotein Changes in Type 2 Diabetes Patients Treated with Empagliflozin.Biomedicines · 2026Article
- Effects of Metformin Monotherapy Versus Metformin Plus SGLT-2 Inhibitor Therapy on Molecular and Cellular Inflammatory Markers in Patients with Newly Diagnosed Type 2 Diabetes Mellitus.Journal of clinical medicine · 2026Article
- Myocardial Lipid Metabolism Imbalance: The Pathological Core and Novel Diagnostic-Therapeutic Directions of Cardiovascular Diseases.Journal of biochemical and molecular toxicology · 2026Review
- Sub1 contributes to heart failure with preserved ejection fraction driven by aging in mice.Nature communications · 2026Article
- Synergistic SGLT2 and GLP-1R targeting alleviates systemic inflammation-induced and M1 monocyte-driven endothelial dysfunction in coronary artery disease.Cardiovascular diabetology · 2026Article
- Effects of Sodium-Glucose Cotransporter-2 Inhibitors on Left Ventricular Global Longitudinal Strain in Adults with Type 2 Diabetes Mellitus: A Systematic Review.Journal of clinical medicine · 2026Review
- Revisiting Insulin Resistance in the Pathophysiology of Type 2 Diabetes Mellitus: A Multi-Organ Perspective.Diabetes & metabolism journal · 2026Review
- Circulating β-Hydroxybutyrate in Glycemic Progression and Diabetic Cardiomyopathy: Adaptive Signal or Maladaptive Substrate?International journal of molecular sciences · 2026Review
- Metabolic inflexibility across heart failure phenotypes: mechanisms and type-specific therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Comparative Effectiveness of Finerenone Versus SGLT2 Inhibitors in Patients with HFpEF and CKD: A Real-World Propensity-Matched TriNetX Analysis.Biomedicines · 2026Article
- Implications of ferritinophagy in cardiovascular diseases and its pharmacological modulation: underlying mechanisms and clinical translation strategies.Cellular & molecular biology letters · 2026Review
- Target trial emulation of sodium glucose cotransporter 2 inhibitors and clinical outcomes in diabetes and end stage kidney disease.Scientific reports · 2026Article
- Prognostic value of potential energy derived from noninvasive pressure-volume loop analysis in heart failure with preserved ejection fraction.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- More than Glucose Elimination: Additional Benefits of SGLT2 Inhibitors in Glomerular Diseases.Drugs · 2026Review
- The role and therapeutic potential of succinate and succinylation in cardiovascular diseases.Clinical epigenetics · 2026Review
- Targeting Skeletal Muscle in Duchenne Muscular Dystrophy: Integrating in Silico and Experimental Approaches to Sodium-Glucose Cotransporter-2 Inhibition.The American journal of pathology · 2026Article
53 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce heart failure events by direct action on the failing heart that is independent of changes in renal tubular function. In the failing heart, nutrient transport into cardiomyocytes is increased, but nutrient utilization is impaired, leading to deficient ATP production and the cytosolic accumulation of deleterious glucose and lipid by-products. These by-products trigger downregulation of cytoprotective nutrient-deprivation pathways, thereby promoting cellular stress and undermining cellular survival. SGLT2 inhibitors restore cellular homeostasis through three complementary mechanisms: they might bind directly to nutrient-deprivation and nutrient-surplus sensors to promote their cytoprotective actions; they can increase the synthesis of ATP by promoting mitochondrial health (mediated by increasing autophagic flux) and potentially by alleviating the cytosolic deficiency in ferrous iron; and they might directly inhibit glucose transporter type 1, thereby diminishing the cytosolic accumulation of toxic metabolic by-products and promoting the oxidation of long-chain fatty acids. The increase in autophagic flux mediated by SGLT2 inhibitors also promotes the clearance of harmful glucose and lipid by-products and the disposal of dysfunctional mitochondria, allowing for mitochondrial renewal through mitochondrial biogenesis. This Review describes the orchestrated interplay between nutrient transport and metabolism and nutrient-deprivation and nutrient-surplus signalling, to explain how SGLT2 inhibitors reverse the profound nutrient, metabolic and cellular abnormalities observed in heart failure, thereby restoring the myocardium to a healthy molecular and cellular phenotype.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.