Atrial fibrillation and chronic kidney disease (CKD) frequently coexist, increasing thromboembolic and bleeding risks. This is a narrative review of pathophysiology and clinical evidence for anticoagulation strategies in CKD patients. Direct oral anticoagulants are preferred in CKD stages 1–4. Recent data suggest that the efficacy of apixaban and rivaroxaban is comparable to that of warfarin in end-stage renal disease. In advanced CKD, anticoagulation should be tailored with close monitoring.

The clinical and genetic characteristics of TMED3, a p24-family protein, across different cancer types remain incompletely understood. This study aimed to evaluate its expression patterns, prognostic relevance, epigenetic regulation, immune associations, genetic alterations, functional networks, and chemical-gene interactions across six cancer types.

Public, de-identified data from UALCAN, GENT2, the Human Protein Atlas (HPA), Kaplan-Meier Plotter, MEXPRESS, cBioPortal, TIMER2.0, the Comparative Toxicogenomics Database (CTD), STRING, and DAVID were analyzed. The clinical and genetic characteristics of TMED3 in bladder cancer (BLCA), head and neck squamous cell carcinoma (HNSC), kidney renal clear cell carcinoma (KIRC), kidney renal papillary cell carcinoma (KIRP), liver hepatocellular carcinoma (LIHC), and lung adenocarcinoma (LUAD) were analyzed. Database-reported nominal P-values were used because unified multiple-testing correction was not feasible.

In UALCAN analysis, TMED3 mRNA was upregulated in BLCA, KIRP, LIHC, KIRC, and LUAD and downregulated in HNSC. HPA data showed higher TMED3 protein expression in BLCA, HNSC, and LUAD. Kaplan-Meier Plotter analysis showed that higher TMED3 expression was associated with shorter overall survival in HNSC, KIRC, KIRP, LIHC, and LUAD, but not in BLCA, and was not significantly associated with recurrence-free survival in any of the six cancers. MEXPRESS analysis suggested an inverse association between promoter methylation and TMED3 expression. TIMER analysis showed negative correlations between TMED3 expression and CD8+ T-cell infiltration in BLCA, HNSC, and LUAD, but a positive correlation in LIHC. cBioPortal showed low TMED3 alteration frequencies across the six cancers, and STRING and DAVID analyses linked TMED3-associated genes mainly to endoplasmic reticulum-Golgi trafficking and vesicle-mediated transport pathways. CTD analysis identified azacitidine, doxorubicin, and MK-2206 as chemicals associated with altered TMED3 expression.

TMED3 is a cancer-type-specific prognostic candidate associated with shorter overall survival in five of the six analyzed cancers. Its transcript-protein discordance, methylation pattern, and immune correlations define testable biological hypotheses, but independent experimental and clinical validation is required before clinical application.

This study aimed to evaluate the predictive value of cholesterol, high-density lipoprotein, and glucose index (CHG index) alone and combined with the monocyte-to-high-density lipoprotein cholesterol ratio (MHR) or triglyceride-to-high-density lipoprotein cholesterol ratio (TG/HDL-C) for NSTE-ACS.

This cross-sectional diagnostic study included 150 patients with NSTE-ACS and 76 healthy controls. Based on the median Gensini score, patients were divided into high-risk (Gensini score ≥51, n = 75) and low-risk groups (Gensini score <51, n = 75). MHR, TG/HDL-C, and CHG index were compared between patients and controls and between high- and low-risk groups. Their correlations with Gensini scores were assessed. Univariate and Multivariate binary logistic regression analysis was performed to identify factors independently associated with high-risk coronary lesions among patients with NSTE-ACS. The predictive performance of individual indicators (MHR, TG/HDL-C, and CHG index) and their combinations was evaluated using receiver operating characteristic curve analysis.

MHR, TG/HDL-C, and CHG index were significantly higher in the patient group than in the control group (all P < 0.001) and the high-risk group than the low-risk group. Those indicators positively correlated with Gensini scores and were independently associated with high-risk coronary lesions among patients with NSTE-ACS (odds ratio (OR) = 16.051, 95% confidence interval (CI): 13.677-99.650 for MHR; OR = 3.562, 95% CI: 1.868-6.793 for TG/HDL-C; and OR = 2.455, 95% CI: 1.040-5.791 for CHG index). The areas under the curve (AUCs) were 0.803 (95% CI: 0.730-0.876) for MHR, 0.746 (95% CI: 0.666-0.826) for TG/HDL-C, and 0.659 (95% CI: 0.573-0.746) for CHG index. The combination of CHG index and TG/HDL-C achieved an AUC of 0.821 (95% CI: 0.755-0.887), while the combination of CHG index and MHR achieved the higher AUC of 0.872 (95% CI: 0.815-0.929).

MHR, TG/HDL-C, and CHG index are independently associated with high-risk coronary lesions among patients with NSTE-ACS. Combining CHG index with MHR or TG/HDL-C shows numerically higher AUCs for identifying high-risk coronary lesions.

Despite the surging global prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) and related liver fibrosis, effective treatments remain limited. While the traditional Chinese medicine Juanyu-Xiaozhi Formula (JYXZF) is used against MASLD, its bioactive components and mechanisms are poorly understood. This study aimed to investigate the therapeutic effects of JYXZF and elucidate its underlying mechanisms of action.

The constituents of JYXZF were characterized using ultra-high-performance liquid chromatography–tandem mass spectrometry (UPLC-MS/MS). Its efficacy was evaluated in a rat model of metabolic dysfunction-associated steatohepatitis (MASH) induced by a high-fat/calorie diet with high-fructose/high-glucose water, utilizing serum biochemistry, histology, and glucose/insulin tolerance tests. Mechanistic validation was performed in free fatty acid-treated human hepatocellular carcinoma cell line HepG2 (HepG2) cells and HepG2/human hepatic stellate cell line LX-2 (LX-2) co-culture models using luciferase assays, chromatin immunoprecipitation-quantitative polymerase chain reaction (ChIP-qPCR), and activator protein 1 (AP-1) overexpression rescue experiments. The functional relevance of stearoyl-CoA desaturase 1 (SCD1) was further assessed in vivo through liver-targeted adeno-associated virus (AAV)-mediated Scd1 overexpression.

Flavonoids were identified as the main bioactive constituents. JYXZF administration alleviated metabolic dysfunction, reduced hepatic lipid accumulation, and attenuated inflammation and fibrosis in MASH rats. Multi-omics integration and machine learning-assisted target prioritization identified lipid metabolic and inflammatory pathways. Among these pathways, we selected the AP-1/peroxisome proliferator-activated receptor gamma (PPARγ)/SCD1-related lipogenic pathway for functional validation. Target perturbation experiments supported the functional involvement of AP-1 in the regulation of the PPARγ/SCD1 pathway and its contribution to the anti-steatotic effects of JYXZF.

JYXZF alleviates MASLD-associated steatosis and fibrosis via the AP-1/PPARγ/SCD1-related lipogenic axis, demonstrating its therapeutic potential for MASLD/MASH and providing a mechanistic basis for future clinical applications.