Cardiovascular disorders are closely linked to metabolic syndrome and remain a leading cause of mortality worldwide, despite advances in early detection and treatment. Adipokines, cardiokines, and myokines play critical roles in maintaining systemic metabolic homeostasis. In this study, we measured serum levels of fatty acid binding protein 4 (FABP4), follistatin-like 1 (FSTL1), irisin, and adiponectin in 243 male patients undergoing elective coronary angiography. We investigated the associations of these biomarkers with coronary artery disease (CAD) and their correlation with metabolic syndrome status. FSTL1 levels were predicted using a Particle Swarm Optimization-enhanced Adaptive Neuro-Fuzzy Inference System (PSO-ANFIS) based on artificial intelligence. Patients with CAD exhibited significantly lower FABP4 levels (p<0.0001), and low FABP4 levels emerged as an independent predictor of CAD in logistic regression analysis (odds ratio 0.903, 95% CI 0.825-0.987, p=0.025). The combination of adiponectin, FSTL1, and irisin as a biomarker strategy demonstrated high sensitivity and specificity for diagnosing metabolic syndrome (AUC = 0.92, 95% CI 0.88-0.96). Both FSTL1 and adiponectin independently correlated with metabolic syndrome (p<0.001, odds ratio 1.039, 95% CI 1.025-1.054; p<0.001, odds ratio 0.979, 95% CI 0.971-0.988, respectively). The prediction of FSTL1 levels using PSO-ANFIS supports the concept of harmonization among metabolic messengers. These findings underscore the potential of FABP4 and FSTL1 as valuable biomarkers for diagnosing metabolic and cardiovascular diseases, thereby facilitating personalized interventions targeting organokine pathways.

Triple-negative breast cancer (TNBC) represents a clinically challenging breast cancer (BC) subtype, characterized by aggressive behavior, high recurrence risk, and limited therapeutic options. MEAK7 has been identified as an alternative mTORC1 signaling pathway regulator; however, its role in BC and TNBC remains uninvestigated. This study aims to assess MEAK7 expression, prognostic significance, and therapeutic potential. We employed public datasets, including TCGA, bc-GenExMiner v5.2, GEPIA3, DOSurvive platforms, Kaplan–Meier Plotter, UALCAN, TIMER2.0, STRING, ENCORI, HPA, miRDB, TargetScan, and CRISPRdb. MEAK7 expression was significantly elevated in BC tissues versus normal breast tissue. MEAK7 expression was pronounced in TNBC and basal-like subtypes, with hypomethylation of its promoter region in TNBC. Elevated MEAK7 expression correlated with reduced disease-free survival (DFS) in TNBC and basal-like. Multivariate Cox regression identified MEAK7 as a significant prognostic factor for overall survival, independent of age and tumor stage. MEAK7 showed CRISPR-targetable gRNA profiles with high on-target efficiency and minimal off-target effects. Analyses revealed negative correlation with tumor-suppressive RNAs (miR-149-3p, miR-135a-5p, and LINC00993) and positive correlation with aggressive regulators (miR-135b-5p and HIF1A-AS2). This study represents one of the initial comprehensive and multi-platform bioinformatic analyses demonstrating that MEAK7 exhibits elevated expression in breast cancer, particularly within the aggressive TNBC. The findings indicate that MEAK7 may serve as a promising prognostic biomarker in TNBC biology and suggest its viability as a molecular candidate for future investigation in targeted therapeutic strategies.

Pancreatic ductal adenocarcinoma (PDAC) is associated with high mortality owing to late diagnosis, aggressive tumor biology, and limited clinically useful early diagnostic and prognostic biomarkers. This study provides an exploratory evaluation of the expression profile, survival associations, co-expressed genes, functional association networks, and regulatory relationships of MEAK7 (KIAA1609/TLDC1) in pancreatic cancer using multi-platform bioinformatic approaches. We conducted a comprehensive multi-platform bioinformatic analysis using multiple publicly available datasets and platforms, including TCGA/GTEx, GEO, GEPIA3, HPA, CPTAC/UALCAN, TNMplot, Kaplan–Meier Plotter, DoSurvive, TIMER 3.0, STRING, TargetScan, miRDB, ENCORI and lncRNADisease. Gene expression patterns, survival associations, immune cell infiltration and regulatory non-coding RNA networks were systematically investigated. A STRING-derived protein functional association network was evaluated. MEAK7 expression patterns were additionally assessed in external GEO datasets, including GSE62165, GSE71729, and GSE183795. In summary, MEAK7 expression was elevated in pancreatic cancer compared with normal pancreatic tissues, was detectably expressed across multiple pancreatic cancer cell lines, and was increased in patient-derived PDAC samples. ROC analysis showed that MEAK7 expression discriminated PDAC tumor tissues from adjacent non-tumor pancreatic tissues, with an AUC of 0.795 (95% CI: 0.719–0.871) indicating exploratory transcriptomic discrimination rather than clinical diagnostic performance. Exploratory survival analyses showed that elevated MEAK7 expression was associated with unfavorable overall survival and disease-free outcomes, while multivariable Cox analyses showed that this association persisted after adjustment for the covariates available within the analyzed dataset. GEO-based analyses supported increased MEAK7 expression in early-stage pancreatic cancer samples, although metastatic expression patterns varied across datasets. Correlation and interaction analyses revealed positive associations between MEAK7 and PDAC-related genes, including CTTN, CDCP1, SMARCA4, SFN, and PALB2, as well as high-confidence STRING functional associations with V-ATPase components and RNASEK. Furthermore, MEAK7 was positively correlated with lncRNA UCA1 and negatively correlated with miR-582-5p. Collectively, these findings identify reproducible expression and survival-associated patterns involving MEAK7 across the analyzed datasets and provide a hypothesis-generating framework for further investigation of its potential biological role in PDAC. Experimental studies and prospectively characterized patient cohorts are required before any clinical, prognostic, diagnostic, or therapeutic implications can be established.

Pulmonary arterial hypertension (PAH) involves complex vascular remodeling. The hypoxia‐inducible factor (HIF) pathway is a central oxygen‐sensing mechanism, but its circulating profile in PAH is poorly defined. This case‐control study included 71 patients with PAH and 93 age‐ and sex‐matched healthy controls. Serum levels of HIF‐1α, HIF‐2α, HIF‐3α, and VHL were measured by ELISA. Serum levels of HIF‐1α, HIF‐2α, HIF‐3α, and VHL were significantly lower in PAH patients compared with controls (all p < 0.05). HIF‐1α demonstrated the highest diagnostic accuracy (AUC: 0.891; 95% CI: 0.836–0.947, p < 0.001). HIF‐2α levels were significantly lower in patients in the intermediate–high risk category compared to the low–intermediate risk category ( p = 0.0449). Circulating HIF pathway proteins are downregulated in PAH. These markers, particularly HIF‐1α and HIF‐2α, show potential for diagnostic screening and risk stratification, suggesting a systemic exhaustion of oxygen‐sensing mechanisms.