Search Results (48)

Background: Branch retinal vein occlusion (BRVO) represents a segmental retinal ischemic disorder characterized by localized oxidative–inflammatory activation. While redox-driven cytokine responses have been described in central retinal vein occlusion, their role in BRVO-specific macular edema and treatment responsiveness remains unclear. This study investigated whether novel redox-related inflammatory mediators in the aqueous humor are associated with disease severity and structural response to anti-vascular endothelial growth factor (VEGF) therapy in BRVO. Methods: Aqueous humor samples were collected from 30 treatment-naïve patients with BRVO and 19 control patients. Levels of VEGF and the novel redox-related inflammatory factors FMS-related tyrosine kinase 3 ligand (Flt-3L), fractalkine, CXCL-16, and endocan-1 were measured by suspension array, and the severity of macular edema was evaluated by measuring central macular thickness and neurosensory retinal thickness (TNeuro) by spectral-domain optical coherence tomography. Therapeutic response was assessed one month after intravitreal ranibizumab injection (IRI). Results: Aqueous levels of VEGF, Flt-3L, and endocan-1 were significantly higher in the BRVO group, and levels of Flt-3L, CXCL-16, and endocan-1—markers associated with oxidative endothelial damage and leukocyte recruitment—correlated significantly with each other and with aqueous flare values. Notably, baseline Flt-3L levels significantly correlated with the reduction in TNeuro, suggesting that this redox-sensitive signaling molecule is a potential biomarker for treatment sensitivity. Conclusions: These findings suggest that novel inflammatory factors, potentially driven by oxidative-nitrosative stress, play a pivotal role in the pathophysiology of BRVO. Baseline Flt-3L may serve as a predictive biomarker for structural responsiveness to anti-VEGF therapy in BRVO, suggesting that oxidative–inflammatory signaling contributes not only to disease severity but also to therapeutic heterogeneity. Full article

Obesity drives chronic low-grade inflammation and endothelial dysfunction, key contributors to subclinical atherosclerosis. This review focuses on the netrin 1/UNC5B axis and its role in promoting macrophage retention within adipose tissue and atherosclerotic plaques, thereby perpetuating local inflammation and vascular injury. Complementary inflammatory markers—including IL 6, hsCRP, and IL 15—are discussed as indicators of systemic inflammatory burden, whereas endocan and ICAM 1 are briefly addressed as markers of endothelial activation. Among emerging pharmacological strategies, glucagon-like peptide-1 receptor agonists (GLP 1RAs) and sodium-glucose cotransporter 2 inhibitors (SGLT2is) show the most consistent evidence for improving these biomarkers and reducing endothelial damage, with GLP 1RAs demonstrating direct effects on carotid intima–media thickness. Integrating biomarker profiling with obesity phenotypes may improve early risk stratification and support more precise management of subclinical atherosclerosis. Full article

Annexin A1 (ANXA1) is a proresolving protein regulated by glucocorticoids, the standard care for severe and critical COVID-19 patients. As part of a larger project including hospitalized COVID-19 patients, this study aimed at evaluating ANXA1 and its FPR2 receptor in these patients, focusing on longitudinal profiles and comparison across disease severities and outcomes, and exploring their correlations with inflammation, endotheliitis and other proresolving mediators. Blood was collected in “severe” (n = 27), “critical” (n = 17) and “critical on veno-venous extracorporeal membrane oxygenation” (n = 17) COVID-19 patients at admission, days 3–4, 5–8, and weekly thereafter, and in controls (n = 23) at a single time point. We quantified ANXA1, resolvin D1, resolvin E1 (RvE1) and endocan by ELISA, cytokines and other endothelial markers by multiplex immunoassays, and FPR2 and Chemerin₁ receptors by RT-qPCR. Most patients underwent a 10-day dexamethasone regimen. Admission ANXA1 and FPR2 were significantly higher in all patient groups. Throughout hospitalization, ANXA1 increased mainly in “severe” patients and survivors, becoming higher at weeks 3 and 4 in survivors versus non-survivors. Variable cumulative dexamethasone doses did not differentially affect ANXA1 or FPR2. ANXA1 was associated with higher RvE1 during the dexamethasone effect period. Exploratory analyses showed that ANXA1 inversely correlated with RvE1 receptor and endotheliitis, whereas both ANXA1 and FPR2 positively correlated with inflammation. In conclusion, ANXA1 may be involved in COVID-19 recovery processes, and its interplay with RvE1 may ameliorate hyperinflammation. Full article

To investigate whether pretreatment serum endocan, platelet-derived growth factor (PDGF)-CC, and -DD levels are elevated in metastatic colorectal cancer (mCRC) patients compared to healthy controls, and to assess their independent associations with chemotherapy response and survival, along with their comparative predictive performance. Adult patients with mCRC receiving systemic chemotherapy combined with an anti-angiogenic agent (bevacizumab or aflibercept) were prospectively enrolled, along with healthy controls. Pretreatment serum samples were collected prior to therapy initiation. Endocan, PDGF-CC, and PDGF-DD levels were measured in duplicate using enzyme-linked immunosorbent assay. Treatment response was evaluated according to Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 and categorized as responders (complete or partial response) and non-responders (stable or progressive disease). Progression-free survival (PFS) and overall survival (OS) were recorded. Median serum levels of endocan (405.5 vs. 269.0 pg/mL), PDGF-DD (499.9 vs. 315.1 pg/mL), and PDGF-CC (2330 vs. 1118 pg/mL) were significantly higher in the mCRC group compared to controls (p < 0.001). In multivariable logistic regression, all three biomarkers were independently associated with non-response to chemotherapy [Odds ratio (ORs): 1.10 for endocan, 1.05 for PDGF-DD, 1.05 for PDGF-CC; all p < 0.05]. For disease progression, Cox regression showed that higher levels of endocan [Hazard ratio (HR) = 1.04], PDGF-DD (HR = 1.03), and PDGF-CC (HR = 1.04) were significant predictors (all p < 0.01). Similar associations were observed for overall mortality (HR = 1.04, 1.02, and 1.02, respectively; all p < 0.05). Endocan, PDGF-DD, and PDGF-CC are elevated in mCRC and independently predict poor treatment response and adverse survival outcomes, highlighting their potential as prognostic biomarkers. Full article

Background/Objectives: This study aimed to investigate the relationship between serum endocan and total testosterone levels in male patients with prediabetes. Materials and Methods: This cross-sectional observational study included 37 men with prediabetes and 37 healthy male controls. In addition to routine laboratory tests, blood samples were collected to measure serum endocan levels using the enzyme-linked immunosorbent assay (ELISA), and total testosterone levels were analyzed using a chemiluminescence method. Results: Age did not differ significantly between the groups (p > 0.05). Body mass index (BMI), fasting plasma glucose (FPG), postprandial plasma glucose (PPG), insulin, HbA1c, and serum endocan levels were significantly higher in the prediabetes group (BMI: p = 0.003; FPG: p < 0.001; PPG: p = 0.019; insulin: p = 0.007; HbA1c: p < 0.001; endocan: p = 0.012). No significant difference was observed in testosterone levels between the groups (p = 0.228). Conclusions: Elevated serum endocan levels in individuals with prediabetes may reflect early endothelial dysfunction associated with glycemic dysregulation. These findings suggest that endocan may serve as an exploratory biomarker of early vascular alterations in prediabetes. However, further large-scale and prospective studies are warranted to clarify its clinical relevance and potential role in risk stratification and the prediction of microvascular complications. Full article

This pilot hypothesis-generating study evaluated whether lipid-related biomarkers (Lp(a), ApoB, and oxLDL), endothelial injury markers (endocan, vimentin), and extracellular matrix glycoproteins (TSP-1, TSP-2) reflect the severity of coronary artery disease (CAD) in patients with stable angina pectoris. 93 patients underwent invasive coronary angiography/coronary CT angiography. CAD severity was evaluated using Gensini, SIS, SSS, and CAD-RADS scores. CAD was confirmed in 76.3% (n = 71). OxLDL correlated with Gensini (r = 0.455; p = 0.006), atherosclerotic segments (r = 0.469; p = 0.005), arteries (r = 0.479; p = 0.004), revascularization indication (r = 0.318; p = 0.003), circumflex artery stenosis (r = 0.323; p = 0.005). OxLDL also correlated with vimentin (r = 0.459; p < 0.001). Vimentin correlated with Gensini (r = 0.480; p = 0.005), SIS (r = 0.349; p = 0.003), SSS (r = 0.320; p = 0.008), CAD-RADS (r = 0.331; p = 0.005), atherosclerotic segments (r = 0.515; p = 0.003), arteries (r = 0.384; p = 0.030), revascularization indication (r = 0.324; p = 0.003). Endocan, TSP-1, and TSP-2 showed no significant associations. These exploratory findings suggest that oxLDL and vimentin may be associated with CAD severity; however, confirmation in larger, prospective cohorts is required. Full article

The pathophysiology of ST-elevated myocardial infarction (STEMI) extends beyond coronary artery occlusion to include microvascular and endothelial dysfunction, both of which critically influence outcomes. Endocan, a soluble dermatan sulfate proteoglycan secreted by endothelial cells, has emerged as a novel biomarker of endothelial activation and dysfunction. Recent studies suggest that elevated endocan levels may carry prognostic significance in patients with STEMI, particularly those undergoing percutaneous coronary intervention (PCI). A comprehensive search of PubMed, Cochrane Library, and Google Scholar was conducted to identify studies evaluating endocan as a prognostic biomarker in STEMI. Review articles, case reports, case series, and experimental studies were excluded. Seven clinical studies, comprising sample sizes ranging from 80 to 320 patients, met the inclusion criteria. Across these studies, endocan levels were analyzed in relation to established prognostic markers and clinical outcomes. Key findings demonstrated that higher endocan levels correlated with stress hyperglycemia (r = 0.21, p < 0.05), higher SYNTAX scores, and worse in-hospital outcomes. A cutoff value of 1.7 ng/mL predicted STEMI with 76.1% sensitivity and 73.6% specificity. Elevated endocan levels also showed positive correlations with the TIMI risk score, major adverse cardiovascular events (MACE), and were identified as independent predictors of incomplete ST-segment resolution (STR) (p = 0.044) and no-reflow phenomenon (NRP) (p < 0.001, OR = 2.39, 95% CI = 1.37–4.15). Collectively, the evidence indicates that endocan is strongly associated with endothelial dysfunction, MACE, NRP post-PCI, and impaired reperfusion. Moreover, traditional prognostic indices such as TIMI and SYNTAX scores appear to correlate with circulating endocan levels. However, variability in reported cutoff values across studies highlights the need for larger, multicenter trials with standardized endpoints to establish endocan’s diagnostic and prognostic utility in STEMI. Full article

Background/Objectives: Awake procedures performed under spinal anesthesia (SA) have been associated with reduced hospitalization, costs, and postoperative complications compared with general anesthesia (GA). Endocan, an endothelial cell-specific proteoglycan, serves as a biomarker of endothelial activation and vascular dysfunction and may reflect the differential vascular and immunomodulatory effects of anesthetic techniques. This prospective observational study aimed to compare perioperative changes in circulating endocan levels between patients undergoing surgery under GA and SA. Methods: Eighty adult patients (aged 18–65 years, ASA I–II) scheduled for elective surgery were included and assigned to GA (n = 42) or SA (n = 38) based on standard clinical indications. Serum endocan levels were measured preoperatively, at 6 h, and at 24 h postoperatively using an ELISA assay. Results: In the GA group, endocan levels increased significantly from baseline (304.5 ± 80.7 pg/mL) to 6 h (511.5 ± 88.7 pg/mL, p < 0.001), and although partially decreased by 24 h (427.5 ± 87.9 pg/mL, p < 0.001), remained above baseline. In the SA group, endocan rose from baseline (320.7 ± 72.5 pg/mL) to 6 h (415.2 ± 79.5 pg/mL, p < 0.001) but returned near baseline at 24 h (352.6 ± 84.7 pg/mL, p = 0.233). Conclusions: These findings suggest that while surgery induces endothelial activation in both groups, GA is associated with a more sustained endothelial response than SA. Full article

Background: Multiple sclerosis (MS) is an immune-mediated neuroinflammatory disorder with a multifactorial etiology involving genetic susceptibility, environmental triggers, and vascular contributions. Carotid intima–media thickness (CIMT) is a significant marker of endothelial dysfunction. Endothelial cell-specific molecule-1 (endocan) and hyaluronic acid, key components implicated in endothelial and vascular remodeling, may significantly contribute to the inflammatory and vascular pathologies observed in MS. We aimed to investigate the relationship between CIMT and endothelial biomarkers, such as endocan and hyaluronic acid, in patients with MS. Methods: In this cross-sectional study, 100 patients with relapsing–remitting MS and 56 healthy controls were included. Demographic, clinical, laboratory, and imaging data were documented. CIMT was measured bilaterally using high-resolution B-mode ultrasonography. Serum endocan and hyaluronic acid levels were quantified via enzyme-linked immunosorbent assays. Results: MS patients exhibited significantly higher CIMT and serum endocan levels compared with controls (p < 0.001). CIMT values were significantly elevated in MS patients, with longer disease duration, higher expanded disability status scale scores, and an older diagnosis age (p < 0.05). However, serum endocan and hyaluronic acid levels did not significantly differ between MS subgroups based on disease duration, disability severity, and diagnosis age. Additionally, there was no correlation between CIMT and serum endocan and hyaluronic acid levels in MS patients (p > 0.05). Conclusions: Increased CIMT and serum endocan levels in MS patients may indicate endothelial dysfunction suggesting vascular involvement in MS. The lack of a correlation between CIMT and endocan and hyaluronic acid levels reveals the complexity of vascular and immune interactions in MS, which needs further research. Full article

Background: Systemic lupus erythematosus (SLE) is an autoimmune disorder associated with premature atherosclerosis and vascular impairment. However, the role of endocan, a biomarker of glycocalyx injury, is not completely clarified in the detection of vascular damage. Therefore, our aim was to investigate serum endocan in comparison with conventional inflammatory markers, arterial stiffness parameters, and carotid ultrasound findings in a cohort of young patients with SLE. Methods: We enrolled 47 clinically active young SLE patients (40 females and 7 males) in the study. Arterial stiffness indicated by augmentation index and pulse wave velocity (PWV) was measured by arteriography. Brachial artery flow-mediated dilatation and common carotid intima-media thickness were detected by ultrasonography. The serum concentrations of endocan, IL-6, MPO, MCP-1, MMP-3, -7, and -9, as well as TNFα, were measured by an enzyme-linked immunosorbent assay (ELISA). Results: We found significant negative correlations between serum endocan and both CH50 and C3. Serum endocan was higher in active SLE patients compared to inactive patients, however, the difference was not statistically significant (241.4 (183–295) vs. 200.3 (167–278) pg/mL; p = 0.313). Serum TNFα and hsCRP significantly correlated with PWV. However, we did not detect significant correlations between vascular diagnostic tests and serum endocan levels. Conclusions: Based on our results, serum endocan is associated with disease activity; however, further studies are needed to clarify the value of serum endocan in the cardiovascular risk estimation of SLE patients. Measurement of serum endocan, as well as the routine assessment of arterial stiffness parameters, should be integrated into the comprehensive management plans of young patients with SLE. Full article

Background: Metabolic syndrome (MetS) is a complex clinical condition characterized by the coexistence of interrelated metabolic abnormalities that significantly increase the risk of cardiovascular diseases and type 2 diabetes mellitus. Endocan—an endothelial cell-specific molecule—is considered a biomarker of endothelial dysfunction and inflammation. This study aimed to evaluate the relationship between serum endocan levels and the severity of MetS, assessed using the MetS-Z score. Methods: This study included 120 patients with MetS and 50 healthy controls. MetS was diagnosed according to the NCEP-ATP III criteria. MetS-Z scores were calculated using the MetS Severity Calculator. Serum levels of endocan, sICAM-1, and sVCAM-1 were measured using the ELISA method. Results: Serum levels of endocan, sICAM-1, and sVCAM-1 were significantly higher in the MetS group compared to the control group (all p < 0.001). When the MetS group was divided into tertiles based on MetS-Z scores, stepwise and statistically significant increases were observed in the levels of endocan and other endothelial markers from the lowest to highest tertile (p < 0.0001). Correlation analysis revealed a strong positive association between the MetS-Z score and serum endocan levels (r = 0.584, p < 0.0001). ROC curve analysis showed that endocan has high diagnostic accuracy for identifying MetS (AUC = 0.967, p = 0.0001), with a cutoff value of >88.0 ng/L. Conclusions: Circulating levels of endocan were significantly increased in MetS and were associated with the severity of MetS, suggesting that endocan may play a role in the cellular response to endothelial dysfunction-related injury in patients with MetS. Full article

Peri- and postmenopausal women often experience unexplained weight gain despite maintaining consistent dietary and lifestyle habits. While the biological mechanisms underlying this phenomenon remain poorly understood, physiological and pathophysiological changes during the menopausal transition are likely contributors. Proteomic profiling holds potential for revealing key molecular pathways involved in the pathogenesis of obesity in this population. This review synthesizes current evidence on proteomic alterations linked to overweight and obesity in peri- and postmenopausal women. A structured literature search was performed across Ovid MEDLINE^®, EMBASE, the Cochrane Library, and Scopus for studies published between October 2010 and March 2025. Eligible studies included original research involving overweight or obese peri- or postmenopausal women that reported proteomic data. Extracted information encompassed study design, participant characteristics, sample types, and proteomic findings. Identified proteins were cross-referenced with a prior review of consistently dysregulated proteins in obesity. Five studies met the inclusion criteria, collectively revealing consistent proteomic patterns associated with inflammation, metabolic dysfunction, and endothelial dysregulation. These included C-reactive protein, Tissue necrotic factor-alpha, interleukins, adiponectin, and endocan. Notably, one study demonstrated that weight loss led to reductions in IL-6, IL-1 receptor antagonist, and CRP, suggesting that obesity-related inflammation may be at least partially reversible. This review provides preliminary evidence linking chronic inflammation, metabolic dysregulation, and vascular stress to obesity in peri- and postmenopausal women. These proteomic signatures enhance understanding of menopausal weight gain and highlight the potential of proteomics to guide personalized interventions. However, larger, well-designed prospective studies are needed to confirm these associations and clarify causal pathways. Full article

Background/Aims: Gastric dysplasia is a critical precursor to gastric cancer (GC), and accurate diagnosis and grading of these lesions are essential for effective surveillance and intervention. However, current diagnostic methods such as forceps biopsy have notable limitations, underscoring the need for reliable biomarkers. This study aimed to evaluate the diagnostic and grading utility of endocan, a soluble proteoglycan secreted by activated endothelial cells, in gastric dysplastic lesions. Methods: A total of 72 patients with gastric dysplasia, 80 with gastric adenocarcinoma, and 55 healthy controls were prospectively enrolled. Endocan expression in gastric tissue samples was assessed via immunohistochemistry and semi-quantitatively graded. Statistical comparisons were made between control, dysplastic (low-grade and high-grade), and malignant groups. Results: Endocan was negatively expressed in all control subjects and positively expressed in 65.3% of the dysplasia group and 100% of the gastric cancer group (p < 0.001). Notably, all high-grade dysplasia cases were endocan-positive, whereas 75.8% of low-grade dysplasia cases were endocan-negative (p < 0.001). Conclusions: This is the first study to demonstrate that endocan is overexpressed in gastric dysplastic lesions. Tissue endocan expression may serve as a practical and robust marker for the diagnosis and grading of gastric dysplasia, potentially enhancing early detection and risk stratification in gastric carcinogenesis. Full article

Background and Objectives: Chronic kidney disease (CKD) is an increasingly significant global public health issue, with cardiovascular disease being the leading cause of mortality. Endothelial dysfunction plays a critical role, but diagnostic tools have certain limitations. Endocan, a soluble proteoglycan, emerged as a promising endothelial dysfunction marker and potential major adverse cardiovascular event (MACE) predictor in haemodialysis (HD) patients. Materials and Methods: In this single-centre, observational, prospective study, non-diabetic HD patients without prior MACEs were monitored. A total of 75 participants met the inclusion criteria. We measured serum endocan, standard biochemical and anthropometric parameters, and parameters of peripheral and central haemodynamics before and after HD in all participants. Results: Patients with higher endocan were older, had elevated CRP and reduced albumin concentrations, and often had a tunnelled central venous catheter (TCVC) for vascular access. Higher serum endocan levels were independently associated with an increased risk of MACEs (aHR = 4.09, 95%-CI: 1.72–9.74), MACE-related mortality (aHR = 2.64, 95%-CI: 1.23–5.66), and all-cause mortality (aHR = 1.86, 95%-CI: 1.07–3.23), both before and after adjusting for predefined confounders, with the highest endocan tercile exhibiting the shortest event-free survival. Conclusions: Endocan is a valuable marker of inflammation and endothelial dysfunction in non-diabetic HD patients. Its elevated concentration indicates an increased cardiovascular risk and more frequent MACEs. Future multicentre studies with repeated endocan assessments should validate its prognostic and diagnostic utility, particularly in long-term patient follow-up. Full article

Background/Objectives: Neonatal early-onset sepsis (EOS) is a life-threatening condition, and numerous efforts have been invested in identifying the most promising biomarkers for its detection. In this prospective cohort study, we aimed to determine the diagnostic accuracy and optimal cut-off values of procalcitonin (PCT), presepsin, endocan, and interleukin (IL)-6 determined from the neonatal serum (0–12, 24–48, and 72–96 h), and umbilical blood cord for the diagnosis of EOS. Methods: A total of 122 patients were included in this study and were divided into two groups: group 1 (sepsis, n = 68 patients) and group 2 (without sepsis, n = 54 patients). Maternal and neonatal characteristics were assessed using descriptive statistics. Logistic regressions were used to evaluate the association between various biomarkers and the presence of EOS and to adjust for potential confounders. Using sensitivity analysis and Youden’s index from the ROC curve, the biomarkers’ diagnostic accuracy and optimal cut-off values were obtained. Results: PCT at 0–12 and 24–48 h of life exhibited the best diagnostic performance, with sensitivities (Ses) of 75% and 76.5% and specificities (Sps) above 74%. Presepsin demonstrated excellent performance at 24–48 h, with Ses of 68.42%, and Sps of 88.89%. IL-6 and endocan achieved modest results for the detection of EOS. Conclusions: PCT and presepsin measured at early neonatal timepoints demonstrated high diagnostic accuracy and favorable sensitivity–specificity balance for predicting EOS. Full article