ReviewEndocrinology and metabolism (Seoul, Korea)2025
SGLT2 Inhibitors as Systemic Metabolic Modulators: Linking Glucose Excretion to Liver Function Restoration.
Review in Endocrinology and metabolism (Seoul, Korea), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis 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
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Comparison of the Efficacy of Denosumab and Alendronate in Improving Bone Mineral Density in Osteoporosis Patients and High-Risk Populations: A Systematic Review and Meta-Analysis.Clinical drug investigation · 2026Pooled it
- Protective effect of dapagliflozin against hepatic ischemia-reperfusion injury in rats.Molecular biology reports · 2026Article
- Immune Determinants of MASLD Progression: From Immunometabolic Reprogramming to Fibrotic Transformation.Biology · 2026Review
- Effects of SGLT-2 inhibitors and GLP-1 receptor agonists on liver function in patients with non-alcoholic fatty liver disease and type 2 diabetes.Frontiers in endocrinology · 2026Observational
- Calcium imbalance drives organelle network collapse and immune remodeling: novel pathogenic mechanisms in MASLD progression.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Sodium-glucose cotransporter 2 (SGLT2) inhibitors have emerged as paradigm-shifting therapeutics that extend beyond glycemic regulation, to conferring profound hepatometabolic benefits. This review delineates the multifaceted mechanisms underlying metabolic dysfunction-associated steatotic liver disease (MASLD), with an emphasis on systemic metabolic remodeling, mitochondrial protection, and intracellular calcium restoration. By promoting glucosuria-induced energy depletion, SGLT2 inhibition alleviates insulin resistance, suppresses hepatic lipogenesis, and activates adenosine monophosphate-activated protein kinase (AMPK)-sirtuin 1 (SIRT1)-peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1α pathways that reprogram hepatocellular metabolism toward achieving lipid oxidation and autophagy. Mechanistically, SGLT2 inhibitors restore intracellular Ca2+ homeostasis via sarcoplasmic/endoplasmic reticulum calcium ATPase 2 (SERCA2) activation, mitigating endoplasmic reticulum (ER) stress and normalizing Ca2+-phosphoinositide (PIP)-protein kinase B (AKT) signaling, collectively reinforcing insulin responsiveness and ER-mitochondrial crosstalk. Clinically, these effects translate into consistently reducing hepatic fat, aminotransferases, and fibrosis markers in both diabetic and nondiabetic patients with MASLD. Furthermore, SGLT2 inhibitors uniquely integrate renal energy regulation with hepatic resilience through the Ca2+-PIP-SERCA axis, positioning them as prototype systemic modulators of metabolic homeostasis. Future translational efforts should refine patient stratification using metabolomic and Ca2+-imaging biomarkers to delineate therapeutic responders and advance next-generation SGLT2 analogs targeting Ca2+-dependent metabolic signaling. Collectively, SGLT2 inhibitors represent a new metabolic therapeutic class that unify glucose, lipid, and Ca2+ regulation to restore hepatocellular functions in metabolic liver diseases.
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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.