Vascular Endothelial Dysfunction Research Articles

MiR-34a-5p/MARCHF8/ADAM10 axis in the regulation of vascular endothelial cell dysfunction and senescence.

miR-34a-5p/MARCHF8/ADAM10 axis in the regulation of vascular endothelial cell dysfunction and senescence.

Malvidin-3-O-glucoside ameliorates the development of vascular endothelial dysfunction in type 2 diabetes mellitus by inhibiting arginase 1 expression

Malvidin-3-O-glucoside ameliorates the development of vascular endothelial dysfunction in type 2 diabetes mellitus by inhibiting arginase 1 expression

Epigallocatechin-3-gallate as an effective inhibitor of vascular endothelial dysfunction induced by endothelial-localized myeloperoxidase.

Epigallocatechin-3-gallate as an effective inhibitor of vascular endothelial dysfunction induced by endothelial-localized myeloperoxidase.

Elevated level of circulating VEGF in Chinese patients with hereditary angioedema and its correlation with disease status

BackgroundHereditary angioedema (HAE) is a rare inherited disease characterized by recurrent, potentially life-threatening angioedema. The vascular endothelium dysfunction is reported to play a role in angioedema episodes. Here, we conducted a case-control study to explore the correlation between vascular endothelium growth factor (VEGF), a representative indicator for endothelium dysfunction, and HAE as well as its attack frequency, disease control and disease severity.MethodsPatients with HAE and non-hereditary angioedema in their attack-free period were prospectively recruited. Demographic and disease information were collected through questionnaires. Disease control of HAE was assessed with the angioedema control test (AECT) with a recall period of three months. The current severity of HAE was comprehensively assessed through frequency of angioedema episodes, occurrence of life-threatening angioedema, necessity for hospitalization or emergency department visits. The plasma VEGF level was measured by chemiluminescence microparticle immunoassay. We compared clinical characteristics between HAE and non-hereditary angioedema patients, as well as among HAE patients with different attack frequency, disease control and disease severity. We further performed several generalized linear models (GLMs) to examine the correlation between VEGF levels and the attack frequency, disease control and disease severity of HAE.ResultsWe enrolled 74 patients with HAE and 55 patients with non-hereditary angioedema. HAE patients exhibited higher VEGF levels in remission than controls (112 vs. 60 ng/ml, P < 0.001). VEGF levels further increased in HAE patients with more frequent angioedema attacks, poorer disease control and greater disease severity. Results of GLMs confirmed significant correlations between plasma VEGF concentrations and the attack frequency of angioedema, disease control status and disease severity of HAE.ConclusionCirculating VEGF level elevated in patients with HAE during attack-free periods, particularly among those with greater disease burden, suggesting the involvement of vascular endothelial dysfunction in the pathogenesis of HAE. VEGF may serve as a predictive biomarker for risk stratification and disease monitoring in HAE.

Dapagliflozin prevents vascular ischemia-reperfusion injury in healthy young males: a randomized, placebo-controlled, double-blinded trial

Ischemia-reperfusion injury (IRI) causes vascular endothelial dysfunction. Preclinical data suggest that the SGLT2 inhibitor dapagliflozin may protect against vascular IRI. This trial has investigated if oral treatment with dapagliflozin can mitigate the transient impairment of IRI-induced-endothelial dysfunction in the forearm resistance vasculature. 32 healthy males (n = 16 per group, age: 27 ± 4 yrs) were studied in this randomized, placebo-controlled, parallel-group, double-blinded trial. Acetylcholine (ACh; endothelium-dependent vasodilator) and glyceryltrinitrate (GTN; endothelium-independent vasodilator) were administered into the brachial artery of the non-dominant arm. The response to stepwise increasing doses on forearm blood flow (FBF) was assessed. FBF was measured before and after a cuff-induced 20-minute forearm ischemia at pre-dose and following daily intake of 10 mg dapagliflozin or placebo over 15 days. IRI reduced endothelium-dependent vasodilatation by 29% (p < 0.001, paired t-test). After a 15-day treatment period, IRI-induced endothelial dysfunction was abrogated in participants receiving dapagliflozin (FBF AChAUC ratios post- vs. pre-ischemia: dapagliflozin: 0.93; 95% CI: 0.80–1.29) but unchanged with placebo (0.81; 95% CI: 0.68–0.92; p = 0.015 vs. pre-ischemia). GTN-induced vasodilation was not altered by IRI or treatment. Dapagliflozin treatment at standard clinical doses over 15 days prevents IRI-induced vascular endothelial dysfunction in the forearm resistance vasculature of healthy young males. The underlying mechanism and the potential clinical impact remain to be demonstrated.Clinical trial registrationhttps://clinicaltrials.gov/study/NCT05217654 NCT05217654; EudraCT number: 2021-005002-95 Date of registration: 20/01/2022.

Mechanisms of vascular endothelial cell injury triggered by blood glucose changes in gestational diabetes mellitus.

The precise pathogenic mechanism of long-term detrimental effects on mothers and infants resulting from gestational diabetes (GDM) remains unclear. This study aimed to examine the long-term detrimental consequences of GDM on mothers and newborns, particularly the impact of glucose concentration variations on vascular endothelial cells and its possible pathogenic mechanisms. An analysis was conducted on the clinical data of 68 healthy pregnant women and 67 pregnant women diagnosed with GDM. Human umbilical vein endothelial cells (HUVECs) were obtained from six pairs of pregnant women for transcriptomic sequencing and analysis, which were concurrently analysed with existing databases. The study examined the effects of varying glucose concentrations on HUVECs, incorporating relevant biological experimental verifications, and assessed oxidative stress, inflammation, and the TGF-β signalling pathway. Clinical data analysis indicated that in patients with gestational diabetes mellitus, early pregnancy hyperglycemia is significantly linked to adverse pregnancy outcomes, even when blood glucose levels are well-controlled. Transcriptomic sequencing revealed significant alterations in the gene expression of HUVECs under GDM conditions, highlighting enrichment in genes associated with metabolism, inflammation, oxidative stress, and diabetes signalling pathways. Cellular experiments indicated that a transition in glucose concentration from elevated to reduced levels can result in damage and dysfunction in HUVECs, elevate ROS levels, and activate the TGF-β signalling pathway. Additionally, injured HUVECs release CTGF through the TGF-β signalling pathway, influencing the extracellular matrix and surrounding cells. The findings demonstrate that alterations in glucose concentration, particularly the shift from high to low levels, can lead to vascular endothelial cell dysfunction, increase ROS levels, and are associated with the TGF β/SMAD3 signalling pathway. Furthermore, compromised HUVECs can influence the microenvironment via their secretions, potentially jeopardising the health of both the mother and foetus.

Tropisetron attenuates high-glucose-induced vascular endothelial dysfunction via inhibition of calcineurin/NFAT signalling.

Tropisetron attenuates high-glucose-induced vascular endothelial dysfunction via inhibition of calcineurin/NFAT signalling.

Emerging Role of Leptin in Vascular and Placental Dysfunction in Preeclampsia.

Leptin is a well-known metabolic hormone that plays diverse roles in various body functions, including growth, reproduction, and blood pressure regulation. In pregnancy, leptin produced from the placenta is crucial for ensuring proper fetal development and angiogenesis; however, pathological increases in leptin in maternal circulation are strongly associated with vascular endothelial dysfunction and preeclampsia. Leptin has a strong role in fertility and healthy pregnancy; however, numerous clinical reports over the last 2 decades show that leptin levels pathologically increase in patients with preeclampsia independent of metabolic status (ie, obesity). Despite this strong correlation, the role of leptin in preeclampsia is largely unexplored compared with other biomarkers likely due to differences in placental leptin production among mammals. Emerging literature has recently begun to shed light on this hormone in preeclampsia pathogenesis and uncovered some key mechanisms whereby pathologically elevated leptin production leads to cardiovascular complications for pregnant women.

SIRT3 suppresses vascular endothelial senescence via DHRS2 and contributes to the anti-vascular aging effect of Bazi Bushen capsule.

Vascular and endothelial aging are significant causes of chronic diseases among the elderly. This study investigated the specific mechanism by which sirtuin 3 (SIRT3) regulates vascular endothelial senescence and the beneficial role of Bazi Bushen capsule (BZBS) in preventing vascular aging. Human umbilical vein endothelial cells and mouse aortic endothelial cells were cultured with D-galactose (D-gal) to induce aging and evaluate the beneficial effects of the SIRT3-dehydrogenase/reductase member 2 (DHRS2) axis on the inhibition of vascular endothelial aging. d-Gal was injected intraperitoneally into wild-type and Sirt3 knockout mice, while BZBS was administered orally. Histochemical staining, immunohistochemistry, and western blotting assays were used to explore the beneficial effects of BZBS against aging-associated vascular remodelling. Endothelial cell function assays were used to evaluate the role of BZBS in suppressing endothelial aging in vitro. SIRT3 deacetylated DHRS2 and modulated the translation of DHRS2. The SIRT3-DHRS2 axis played an important role in preserving mitochondrial homeostasis and reducing reactive oxygen species generation through suppressing endothelial nitric oxide synthase (eNOS) translocating to mitochondria and eNOS-Thr495 phosphorylation mediated by protein kinase C δ (PKCδ). BZBS mitigated vascular remodelling and relieved endothelial oxidative stress via the SIRT3-DHRS2 axis. SIRT3 activates DHRS2-PKCδ to stop aging in endothelial cells by inhibiting uncoupled eNOS translocating to mitochondria. BZBS rescued vascular aging and endothelial dysfunction via the SIRT3-DHRS2 axis. Revealing a protective mechanism by which SIRT3 inhibits endothelial senescence, this study provides evidence for BZBS in delaying vascular aging.

Herbal-based Xuebijing injection ameliorated vascular endothelial dysfunction via inhibiting ACLY/MYB/RIG-I axis in sepsis-associated lung injury.

Herbal-based Xuebijing injection ameliorated vascular endothelial dysfunction via inhibiting ACLY/MYB/RIG-I axis in sepsis-associated lung injury.

Vascular remodeling and endothelial dysfunction in patients with occupational chronic obstructive pulmonary disease caused by exposure to industrial aerosol nanoparticles

BACKGROUND: The characteristics of vascular pathology in different phenotypes of occupational chronic obstructive pulmonary disease (COPD), as well as the causal role of various industrial aerosol components, especially nanoparticles, are poorly understood. AIM: To determine the characteristics of arterial remodeling and endothelial function in patients with occupational COPD caused by exposure to aerosol nanoparticles. METHODS: An observational, cohort cross-sectional study was performed in patients with occupational COPD caused by exposure to aerosols containing metal (n = 48) or silicon (n = 55) nanoparticles, compared with COPD caused by tobacco smoking (n = 50). Scanning electron microscopy and inductively coupled plasma atomic emission spectroscopy were used to measure the size and chemical composition of particles, respectively. The procedures used in the study included color-flow duplex scanning of the brachiocephalic arteries, brachial arteries, and aorta; flow-mediated dilation test of the brachial arteries; and enzyme-linked immunosorbent assay of molecular markers. Linear regression was used to determine relationships. RESULTS: The group of occupational COPD caused by aerosols with silicon nanoparticles had the highest values of carotid intima-media thickness: 1.2 [0.9; 1.5] mm; in the group of occupational COPD caused by aerosols with metal nanoparticles and the control group, these values were 0.9 [0.7; 1.0] mm and 0.8 [0.7; 0.9] mm, respectively (p = 0.009). Moreover, the group of occupational COPD caused by aerosols with silicon nanoparticles had the highest incidence of atherosclerosis compared to the group of occupational COPD caused by aerosols with metal nanoparticles and the control group (41.8% vs. 22.9% and 18.0%, respectively; р = 0.003). The aortic pulse wave velocity in the three groups was 12.6 [11.2; 14.1], 9.3 [8.9; 10.7], and 7.2 [6.9; 8.4] m/s, respectively (р = 0.001). The minimum flow-mediated dilation of the brachial arteries was 2.5 [2.1; 3.4], 3.8 [3.3; 4.6], and 4.7 [4.5; 5.3]%, respectively (р = 0.001). Occupational COPD caused by aerosols with silicon nanoparticles was associated with the highest serum levels of vascular cell adhesion molecule 1, von Willebrand factor, transforming growth factor β1, procollagen III N-terminal propeptide, and fibroblast growth factor 2. Regression relationships were found between the intima-media thickness and the concentration of metal (adjusted R-squared [R2]: 0.36) and silicon (adjusted R2: 0.47) nanoparticles, as well as the length of employment (adjusted R2: 0.27). Moreover, regression relationships were found between the flow-mediated dilation of the brachial arteries and the concentration of metal (adjusted R2: 0.51) and silicon (adjusted R2: 0.71) nanoparticles, the length of employment (adjusted R2: 0.68), and the total concentration of silicon-containing dust (adjusted R2: 0.55). CONCLUSION: Occupational COPD caused by exposure to aerosol nanoparticles (especially silicon-containing ones) is associated with significant vascular remodeling and endothelial dysfunction, which must be considered during follow-up care.

Efficiency and safety of the integrated use of medical gases thermal heliox, nitric oxide and molecular hydrogen in patients with exacerbation of chronic obstructive pulmonary disease complicated by hypoxemic, hypercapnic respiratory failure and secondary pulmonary arterial hypertension in the post-COVID period

To study the efficacy and safety of the combined use of thermal heliox (t-He/O2), nitric oxide (NO) and molecular hydrogen (H2) in patients with exacerbation of chronic obstructive pulmonary disease (COPD) complicated by hypoxemic, hypercapnic respiratory failure (RF) and secondary pulmonary arterial hypertension (PAH) in the post-COVID period. The randomized, comparative, controlled, parallel study included patients (n=100, 52 men and 48 women) with exacerbation of COPD levels of evidence C and D (GOLD 2021-2023) with hypoxemic, hypercapnic respiratory failure and secondary PAH, who had pneumonia caused by SARS-CoV-2 before hospitalization. Patients with similar demographic, clinical, and functional parameters, who received non-invasive ventilation (NIV) and oxygen (O2) along with standard drug therapy, were divided into 5 groups: Group 1 (main): (n=22: 12 men, 10 women, who received t-He/O2, NO, and H2 sequentially); Group 2 (n=20: 10 men, 10 women, who received t-He/O2 and NO); Group 3 (n=20: 11 men, 9 women, who received t-He/O2 and H2); Group 4 (n=18: 10 men, 8 women, who received NO and H2); Group 5 (control) (n=20: 9 men, 11 women). The dynamics of the clinical condition of patients, gas exchange in the lungs, acid-base balance, left-to-right discharge fraction, hemodynamic parameters, and exercise tolerance were assessed. A positive effect of the complex use of medical gases on the clinical condition of patients, gas exchange parameters in the lungs, metabolism, hemodynamic parameters and exercise tolerance was found in comparison with these parameters in patients who received medical gases separately and with the control group. The combination of t-He/O2, NO and H2 with simultaneous pathogenetic therapy and NIV in patients with exacerbation of COPD complicated by hypoxemic, hypercapnic RF and secondary PAH in the post-COVID period is safe and more effective compared to groups receiving each medical gas separately. Complex therapy improves the clinical condition of patients, reduces signs of hypoxemia and hypercapnia, vascular endothelial dysfunction, metabolic disorders and increases tolerance to physical activity by normalizing gas exchange in the lungs, increasing oxygen delivery to tissues, reducing the shunt fraction, and restoring metabolism.

A Systematic Review of Endothelial Dysfunction in Chronic Venous Disease-Inflammation, Oxidative Stress, and Shear Stress.

Chronic venous disease (CVD) is among the most common diseases in industrialized countries and has a significant socioeconomic impact. The diversity of clinical symptoms and manifestations of CVD pose major challenges in routine diagnosis and treatment. Despite the high prevalence and the huge number of venous surgical interventions performed every day, a substantial proportion of the etiopathogenesis remains unclear. There are several widely advocated and generally valid theories of "peri-capillary fibrin cuffs" and "white cell trapping hypothesis", which consider the role of venous reflux/obstruction, inflammation, vascular remodeling, hemodynamic changes, genetic and social risk factors. There are several specific provoking factors for the development of venous reflux: incompetence of the valve system, inflammation of the vascular wall, and venous hypertension. Over the past few years, increasing scientific data has demonstrated the link between oxidative stress, endothelial dysfunction, and vascular inflammation. High levels of oxidants and persistent inflammation can cause cumulative changes in hemodynamics, resulting in permanent and irreversible damage to the microcirculation and endothelial cells. Production of reactive oxygen species and expression of inflammatory cytokines and adhesion molecules are involved in a vicious cycle of venous wall remodeling. The interaction of ROS, and in particular, the superoxide anion radical, with nitric oxide leads to a decrease in NO bioavailability, followed by the initiation of prolonged vasoconstriction and hypoxia and impairment of vascular tone. This review addresses the role of ED, oxidative, and hemodynamic stress in the CVD mediation. Based on predefined inclusion and exclusion criteria, we conducted a systematic review of published scientific articles using PubMed, PMC Europe, Scopus, WoS, MEDLINE, and Google Scholar databases in the interval from 24 April 2002 to 1 April 2025. The current review included studies (n = 197) scientific articles, including new reviews, updates, and grey literature, which were evaluated according to eligibility criteria. The selection process was performed using a standardized form according to PRISMA rules, the manual search of the databases, and a double-check to ensure transparent and complete reporting of reviews. Studies had to report quantitative assessments of the relationship between vascular endothelial dysfunction, inflammation, oxidative stress, and shear stress in a chronic venous disease.

AhR Activation at the Air-Blood Barrier Alters Systemic microRNA Release After Inhalation of Particulate Matter Containing Environmentally Persistent Free Radicals

Particulate matter containing environmentally persistent free radicals (EPFRs) is formed when organic pollutants are incompletely burned and adsorb to the surface of particles containing redox-active metals. Our prior studies showed that in mice, EPFR inhalation impaired vascular relaxation in a dose- and endothelium-dependent manner. We also observed that activation of the aryl hydrocarbon receptor (AhR) in the alveolar type-II (AT-II) cells that form the air-blood interface stimulates the release of systemic factors that promote endothelial dysfunction in vessels peripheral to the lung. AhR is a recognized regulator of microRNA (miRNA) biogenesis, and miRNA control diverse signaling pathways. We thus hypothesized that systemic EPFR-induced vascular endothelial dysfunction is initiated via AhR activation in AT-II cells, resulting in a systemic release of miRNA. Using a combustion reactor, we generated EPFR of two free radical concentrations—EPFRlo (1016–17 radicals/g particles) and EPFR (1018–19 radicals/g)—and exposed mice by inhalation. EFPR inhalation resulted in changes in a distinct array of miRNA in the plasma, and these miRNAs are linked to multiple systemic effects, including cardiovascular diseases and dysregulation of cellular and molecular pathways associated with cardiovascular dysfunction. We identified 17 miRNA in plasma that were altered dependent upon both AhR activation in AT-II cells and ~ 280 ug/m3 EPFR exposure. Using Ingenuity Pathway Analysis, we found that 5 of these miRNAs have roles in modulating endothelin-1 and endothelial nitric oxide signaling, known regulators of endothelial function. Furthermore, EPFR exposure reduced the expression of lung adherens and gap junction proteins in control mice but not AT-II-AhR deficient mice, and reductions in barrier function may facilitate miRNA release from the lungs. In summary, our findings support that miRNA may be systemic mediators promoting endothelial dysfunction mediated via EPFR-induced AhR activation at the air-blood interface.Graphical

Therapeutic Potential of Hexahydrocurcumin in the Regeneration and Protection of the Retinal Pigment Epithelium.

Hexahydrocurcumin (HHC), the primary metabolite of curcumin, shows promising therapeutic potential due to its antioxidant and anti-inflammatory properties. The retinal pigment epithelium (RPE) plays a crucial role in maintaining retinal homeostasis; however, its dysfunction-linked to oxidative stress and chronic inflammation-contributes to the progression of degenerative diseases such as age-related macular degeneration (AMD). This review highlights the therapeutic potential of HHC in protecting and regenerating RPE cells. It explores the effects of oxidative stress on the RPE, the mechanisms underlying its damage, and the involvement of reactive oxygen species (ROS) and inflammatory mediators. HHC has demonstrated the ability to modulate these pathways by activating nuclear factor erythroid 2-related factor 2 (NRF2), enhancing antioxidant defenses, and inhibiting pro-inflammatory cytokine production. Preclinical studies suggest that HHC mitigates vascular remodeling and endothelial dysfunction by reducing the expression of transforming growth factor β (TGF-β1) and matrix metalloproteinase-9 (MMP-9). Moreover, HHC improves nitric oxide bioavailability and promotes nitric oxide synthase expression, thereby counteracting oxidative stress-induced vascular damage. Emerging evidence indicates that HHC may be a promising candidate for the treatment of retinal degenerative diseases, particularly those associated with oxidative stress and inflammation. However, further studies, including clinical trials, are essential to confirm its efficacy and elucidate the precise mechanisms underlying HHC's protective effects on RPE cells.

Efficacy and safety of the combined use of medical gases – thermal heliox, nitric oxide and molecular hydrogen – in patients with exacerbation of chronic obstructive pulmonary disease complicated by hypoxemic, hypercapnic respiratory failure and secondary pulmonary arterial hypertension in the post-COVID period

The interest in medical gases for the correction of respiratory failure (RF) has been growing over recent years. However, there are virtually no scientific studies of combination therapy for exacerbation of chronic obstructive pulmonary disease (COPD), which is a combination of non-invasive ventilation (NIV) with thermal heliox (t-He/O2), nitric oxide (NO2) and molecular hydrogen (H2), in the Russian Federation and in the world. The aim of the study was to investigate the efficacy and safety of the combined use of t-He/O2, NO and H2 in patients with exacerbation of COPD complicated by hypoxemic, hypercapnic RF and secondary pulmonary hypertension (PH) in the post-COVID period. Methods. The randomized, comparative, controlled, parallel-group, prospective study included 100 patients (52 men, 48 women) with exacerbation of COPD categories C and D according to the criteria of the Global Initiative for Chronic Obstructive Lung Disease (GOLD, 2021 – 2023), with hypoxemic, hypercapnic respiratory failure and PH, who had COVID-19 (COronaVIrus Disease 2019) complicated by pneumonia caused by SARS-CoV-2 (Severe Acute Respiratory Syndrome-related CoronaVirus 2) before the hospitalization. Patients with similar demographic, clinical, and functional parameters, who received, along with standard drug therapy, NIV in the spontaneous-forced biphasic positive airway pressure (BiPAP S/T) mode and oxygen (O2) to maintain blood hemoglobin oxygen saturation (SpO2) in the range of 95–97% according to GOLD (2021 – 2023), were divided into 5 groups: patients of the 1st (main) group (n = 22: 12 men, 10 women) received t-He/O2, NO, and H2 sequentially; the 2nd group (n = 20: 10 men, 10 women) – t-He/O2 and NO; the 3rd group (n = 20: 11 men, 9 women) – t-He/O2 and H2; the 4th group (n = 18: 10 men, 8 women) – NO and H2; the 5th group (control) (n = 20: 9 men, 11 women) – only standard drug therapy, NIV and O2. Changes in the clinical condition of the patients, gas exchange in the lungs, acid-base balance, left-to-right shunt fraction, hemodynamic parameters, and exercise tolerance (ET) were assessed. Results. Not only clinical condition of the patients, but also the arterial blood gas composition, acid-base balance and intrapulmonary blood shunt fraction, hemodynamics and ET were improved in the main group compared to those in patients who received inhalation therapy with medical gases separately and the control group. Conclusion. The combination of t-He/O2, NO and H2 combined with pathogenetic therapy and NIV in patients with exacerbation of COPD complicated by hypoxemic, hypercapnic DN and secondary PH in the post-COVID period is safe and more effective compared to administering each medical gas separately. The clinical condition of patients improves, signs of hypoxemia and hypercapnia, vascular endothelial dysfunction, and metabolic disorders are reduced with the combined therapy. An increase in ET was also noted due to the normalization of gas exchange in the lungs, increased oxygen delivery to tissues, a decrease in the shunt fraction, and restoration of metabolism.

Endometriosis, Raynaud's Syndrome, and Migraine: A Retrospective Study of 12 Million Women.

Our study focused on evaluating a possible relationship between endometriosis, Raynaud's syndrome, or migraine among women. This was a cross-sectional population-based study. Participants/Materials; Setting; Methods: We used 12,684,067 hospitalized patient records in the Healthcare Cost and Utilization Project (HCUP) database between 2007 and 2014. We calculated the prevalence of endometriosis, Raynaud's syndrome, and migraine. We also evaluated the possible role of depression, anxiety, and autoimmune diseases to eliminate confounding factors. Unadjusted and adjusted multivariate logistic regressions were applied to evaluate the relationship between variables. Unadjusted analysis revealed a strong association between endometriosis and Raynaud's syndrome and migraine (OR = 2.491; 95% CI: 1.677-3.699). After adjusting for sociodemographic characteristics as well as depression and anxiety, the association remained significant (OR = 1.779; 95% CI: 1.166-2.716). Among younger patients aged 18-35 with endometriosis, the associations were stronger with Raynaud's syndrome (adjusted OR = 1.61, 95% CI = 1.20-2.16) and migraine (adjusted OR = 2.59, 95% CI = 2.47-2.72). The HCUP database is cross-sectional in nature, and hence, we could not establish the temporal relationship between endometriosis, Raynaud's syndrome, and migraine. Also, the severity of endometriosis and the treatment received by the patients were not included in the dataset, and it prevented us from investigating the role of potential confounding factors. Our study suggests an association between endometriosis, Raynaud's syndrome, and migraine. It is possible that these conditions share a similar mechanism possibly vascular reaction and endothelial dysfunction related to chronic inflammation.

Role of the endothelial cell glycocalyx in sepsis-induced acute kidney injury.

Sepsis-induced acute kidney injury (S-AKI) is a common complication of sepsis. It occurs at high incidence and is associated with a high level of mortality in the intensive care unit (ICU). The pathophysiologic mechanisms underlying S-AKI are complex, and include renal vascular endothelial cell dysfunction. The endothelial glycocalyx (EG) is a polysaccharide/protein complex located on the cell membrane at the luminal surface of vascular endothelial cells that has anti-inflammatory, anti-thrombotic, and endothelial protective effects. Recent studies have shown that glycocalyx damage plays a causal role in S-AKI progression. In this review, we first describe the structure, location, and basic function of the EG. Second, we analyze the underlying mechanisms of EG degradation in sepsis and S-AKI. Finally, we provide a summary of the potential therapeutic strategies that target the EG.

Anthracyclines-Induced Vascular Endothelial Dysfunction in Cancer Patients and Survivors Using Brachial Flow-Mediated Dilation (FMD) Tool: A Systematic Review and Meta-Analysis

Anthracyclines are effective antineoplastic drugs; however, their use is constrained by dose-dependent cardiotoxicity. Vascular endothelial dysfunction is an early independent event in cardiovascular diseases and may precede anthracycline-induced cardiotoxicity. Brachial flow-mediated dilation (FMD) is a non-invasive technique for evaluating vascular endothelial function. We evaluated the evidence on anthracycline-induced vascular endothelial dysfunction in cancer patients and survivors using FMD. Studies measuring FMD in anthracycline-treated active cancer patients or survivors were retrieved from inception to August 2024 using PubMed, Embase, and Scopus. The primary outcome was the difference in FMD between anthracycline-treated patients and healthy controls or baseline. We performed the meta-analysis using a random-effects model and evaluated the certainty in effect estimates. Overall, 18 studies (n = 841 patients) met the inclusion criteria. Compared to the baseline, a non-significant change toward a decline in FMD was observed. However, a significant reduction in FMD was observed in anthracycline-treated patients compared to healthy controls (standardized mean difference (SMD): − 0.6082; 95% CI: − 0.8963 to − 0.3201; p < 0.0001). Subgroup analyses revealed consistent significant reductions in FMD for childhood cancers (SMD: − 0.7189; 95% CI: − 0.9903 to − 0.4476; p < 0.0001), while adult cancers showed no significant difference. No significant publication bias was detected overall for healthy control comparisons. High heterogeneity was observed in the included studies (I2 = 81.7808% versus healthy controls and I2 = 75.6876% for childhood cancers subgroup analysis). Anthracyclines induce vascular endothelial dysfunction, indicated by lower FMD in cancer patients and survivors, particularly among those with childhood cancers, who might be at risk of long-term cardiovascular complications.

Transport and action of sesame protein-derived ACE inhibitory peptides ITAPHW and IRPNGL.

Transport and action of sesame protein-derived ACE inhibitory peptides ITAPHW and IRPNGL.