ReviewMolecular biomedicine2026
SGLT2 inhibitors: mechanisms, physiology and pharmacology, and clinical applications.
Review in Molecular biomedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Sodium-glucose cotransporter 2 (SGLT2) is a low-affinity, high-capacity transporter expressed predominantly in the renal proximal tubule, where it mediates the sodium-coupled reabsorption of most filtered glucose. SGLT2 inhibitors have evolved from glucose-lowering agents into disease-modifying therapies across the cardio-renal-metabolic continuum. Blockade of proximal tubular transport induces glycosuria, osmotic diuresis, restoration of tubuloglomerular feedback, resetting of renal haemodynamics, and altered fluid compartmentalisation. These early renal and circulatory effects interact with systemic metabolic adaptations, including pseudo-starvation signalling, erythropoiesis, altered uric acid handling, and changes in substrate availability. At the cellular level, SGLT2 inhibition has been linked to improved ionic homeostasis and mitochondrial quality control, reduced oxidative stress, modulation of inflammation, and attenuation of maladaptive tissue remodelling. Endothelial injury may connect these cellular effects with microvascular dysfunction and fibrosis. Endothelial dysfunction and endothelial-to-mesenchymal transition (EndMT) offer a mechanistic framework for understanding the relationship between microvascular injury and fibrosis. However, EndMT is best viewed as one component of a broader endothelial-stromal stress response rather than as a single proven mediator of clinical benefit. These pharmacodynamic and cellular effects help explain the consistent clinical efficacy of SGLT2 inhibitors across type 2 diabetes, chronic kidney disease, and heart failure (HF), while also informing emerging applications in acute HF, after myocardial infarction, and in patients with arrhythmia or metabolic dysfunction-associated steatohepatitis. This Review integrates mechanistic, pharmacological, and clinical evidence to identify unresolved translational gaps and future directions, including mechanism-informed biomarkers, imaging, spatial multi-omics, phenotype-guided patient stratification, dual sodium-glucose cotransporter 1/2 inhibition, and rational combination therapy.
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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.