Chronic kidney disease (CKD) involves inflammation, oxidative stress, and fibrosis, leading to renal dysfunction. Dapagliflozin, an SGLT2 inhibitor, shows renoprotective effects beyond glucose control, but its precise molecular mechanisms remain unclear. This study utilizes network pharmacology and molecular docking to elucidate its multi-target effects in CKD. Dapagliflozin’s SMILES structure was analyzed for ADMET properties. Potential targets were identified via SwissTargetPrediction, GeneCards, and SEA, and common CKD-related targets were determined. A protein–protein interaction (PPI) network was constructed, and key pathways were identified using GO and KEGG enrichment analyses. Molecular docking was conducted to validate dapagliflozin’s binding affinities with hub proteins. A total of 208 common targets were identified, including EGFR, GSK3β, and IL-6. GO and KEGG analyses highlighted key pathways, such as PI3K-Akt, MAPK, and AGE-RAGE, involved in inflammation, oxidative stress, and metabolic regulation. Molecular docking confirmed strong binding affinities with EGFR (−8.42 kcal/mol), GSK3β (−7.70 kcal/mol), and IL-6 (−6.83 kcal/mol). Dapagliflozin exhibits multi-target therapeutic potential in CKD by modulating inflammation, oxidative stress, and metabolic pathways. This integrative approach enhances the understanding of its mechanisms, supporting future experimental validation and clinical application in CKD management.

Acute kidney injury (AKI) is characterized by rapid loss of renal function due to oxidative stress, inflammation, and apoptosis, with limited targeted therapies. Alpha-mangostin (AM), a natural compound from Garcinia mangostana, exhibits antioxidant and anti-inflammatory properties in preclinical studies, but its efficacy in AKI has not been reviewed. This systematic review and meta-analysis, registered on the Open Science Framework and adhering to PRISMA guidelines, analyzed in vivo and in vitro studies on AM’s effects in AKI models through searches of PubMed, Scopus, Embase, and Web of Science. Primary outcomes included serum creatinine and cell viability, while secondary outcomes encompassed oxidative stress markers (malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS)), inflammatory cytokines, apoptosis indicators, and histopathology. Data were extracted independently and assessed using the Toxicological Data Reliability Assessment Tool (ToxRTool). AM significantly reduced serum creatinine (mean difference (MD) = −0.67 mg/dL; 95% confidence interval (CI): −1.28 to −0.06; p = 0.03) and improved cell viability (MD = 28.26%; 95% CI: 17.25 to 39.26; p < 0.0001). It markedly decreased MDA and ROS, increased GSH, and enhanced antioxidant enzymes (glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD)). In vivo, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were lowered, and histopathology showed reduced tubular necrosis and structural damage. Subgroup analyses indicated dose- and model-dependent effects, with lower doses often yielding greater benefits. Sensitivity analyses confirmed robustness despite heterogeneity. Preclinical evidence supports AM’s nephroprotective potential and underscores the need for dose optimization, mechanistic validation, and clinical translation.

Chronic kidney disease (CKD) is a progressive global health challenge. While empagliflozin, a selective SGLT2 inhibitor, is known to attenuate CKD progression through mechanisms beyond glycemic control, the precise molecular pathways remain incompletely characterized and warrant further investigation. This study employed an integrated network pharmacology and molecular docking approach to elucidate the multi-target mechanisms of empagliflozin in CKD. Initial evaluation demonstrated that empagliflozin exhibits favorable physicochemical properties, drug-likeness, and ADMET profiles, supporting its potential as an effective orally administered therapeutic option for CKD management. Network analysis identified 221 shared molecular targets between empagliflozin and CKD-associated genes. Topological analysis of the protein–protein interaction (PPI) network revealed ten critical hub proteins—GAPDH, IL6, EGFR, HSP90AA1, NFKB1, HSP90AB1, MTOR, MAPK3, IL2, and PIK3CA—which serve as key regulators in CKD pathophysiology. Gene Ontology and KEGG pathway enrichment analyses indicated that these shared targets are significantly involved in phosphorylation, signal transduction, and central signaling cascades associated with CKD progression, including the PI3K-Akt, FoxO, HIF-1, and AGE-RAGE pathways. Molecular docking simulations corroborated empagliflozin’s multi-target affinity, demonstrating particularly strong binding energies toward HSP90AB1 (−10.85 kcal/mol), MAPK3 (−9.46 kcal/mol), and EGFR (−9.38 kcal/mol). Empagliflozin maintained stable hydrogen bonding throughout the 200-ns molecular dynamics simulation, primarily with GLN18, GLU42, SER45, ASN46, ASN101, GLY130, and TYR134, underscoring its persistent and well-anchored interaction with HSP90AB1. Collectively, these findings provide crucial mechanistic insights, suggesting that empagliflozin might exerts therapeutic effects by modulating interconnected pathways regulating inflammation, oxidative stress, and metabolic homeostasis, thereby reinforcing its role as a comprehensive, multi-target therapeutic strategy for CKD management. Nonetheless, validation through in vitro experiments remains necessary.

Diabetes mellitus, particularly type 2 diabetes mellitus, is a growing global health burden characterized by chronic hyperglycemia and insulin resistance. Alpha-mangostin (AM), a xanthone from Garcinia mangostana pericarp, exhibits antioxidant, anti-inflammatory, and metabolic regulatory properties in preclinical models. We performed a systematic review and meta-analysis of controlled in vivo studies to assess AM’s anti-hyperglycemic effects. Fourteen studies (25 comparisons) in rodent models of diabetes or hyperglycemia were included. Primary outcome was blood glucose; secondary outcomes were glycated hemoglobin (HbA1c), insulin, and homeostatic model assessment of insulin resistance (HOMA-IR). Random-effects meta-analysis demonstrated that AM significantly reduced fasting blood glucose (mean difference (MD) = −8.75 mmol/L; 95% CI: −10.73 to −6.78; p < 0.001) and HbA1c (MD = −2.20%; 95% CI: −3.07 to −1.32; p < 0.001). AM did not significantly alter circulating insulin (Hedges’ g = 0.43; 95% CI: −0.62 to 1.49; p = 0.42) but improved insulin resistance as measured by HOMA-IR (MD = −0.90; 95% CI: −1.68 to −0.12; p = 0.02). Subgroup, sensitivity, and risk-of-bias analyses supported the robustness of the glucose-lowering association, although substantial between-study heterogeneity was present. Overall, this study provides preclinical evidence that AM exerts significant antihyperglycemic and insulin-sensitizing effects, supporting its potential as a multitarget metabolic modulator. Further standardized and mechanistically informed studies are warranted to facilitate translational progression.

Chronic kidney disease (CKD) requires assessment of both glomerular filtration and kidney damage, particularly albuminuria, for diagnosis, risk stratification, and longitudinal care. Point-of-care testing (POCT) can shorten turnaround time and improve access when conventional laboratory testing is unavailable or would delay a clinical pathway. This narrative review summarizes established and emerging POCT approaches for kidney assessment in CKD, with emphasis on creatinine/eGFR and urine albumin-to-creatinine ratio (UACR), and distinguishes analytical validity from workflow utility and patient-level clinical utility. Evidence is strongest for rapid creatinine measurement in selected workflows, especially pre-imaging assessment and decentralized screening, while quantitative/semiquantitative UACR POCT can support CKD detection when abnormal results are appropriately confirmed. Cystatin C microfluidic systems remain investigational, and kidney injury/stress or molecular biomarkers such as NGAL, KIM-1, L-FABP, [TIMP-2]·[IGFBP7], extracellular vesicles, and microRNAs should be regarded primarily as a research horizon rather than direct measures of GFR. Important implementation requirements include assay-specific validation, calibration traceability, quality assurance, recognition of biological and analytical interference, and confirmation of results near major clinical decision thresholds. Evidence that POCT improves long-term CKD outcomes, safety, adherence, or cost-effectiveness remains limited. Future studies should prioritize prospective clinical utility, implementation, cost-effectiveness, home-use validation, and patient-centered outcomes.

Type 2 diabetes mellitus (T2DM) is often linked to metabolic dysfunction-associated steatotic liver disease (MASLD), a metabolic liver condition defined by excessive lipid deposition within hepatocytes and is frequently accompanied by increased circulating liver enzyme levels. Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as linagliptin, may exert pleiotropic effects on hepatic metabolism; however, their effects on liver enzyme profiles remain uncertain. This systematic review and meta-analysis aimed to evaluate the impact of linagliptin on liver enzymes, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT), in patients with T2DM. A systematic literature search was performed across five electronic databases up to 11 May 2026 following the PRISMA 2020 guidelines. Randomized controlled trials and cohort studies were included, and pooled mean differences (MDs) were calculated using random-effects models. Eight studies involving 1262 participants were analyzed. Linagliptin was associated with a modest reduction in AST (MD −1.58 U/L, 95% CI −2.85 to −0.31) with low heterogeneity, whereas the change in ALT was not statistically significant (MD −1.86 U/L, 95% CI −4.14 to 0.42), and substantial heterogeneity was observed. No significant effects were observed for GGT, while evidence for ALP was limited to a single study and was insufficient to determine the effect of linagliptin. Overall, linagliptin demonstrated limited and inconsistent effects on liver enzyme profiles.