Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Objective: The potential contribution of asymmetric dimethylarginine (ADMA) and high-sensitivity C reactive protein (hsCRP) to endothelial dysfunction in APS patients has not been studied in detail, until now. The study involved 105 APS patients (59 diagnosed with primary APS (PAPS) and 46 APS associated with systemic lupus erythematosus (SAPS)) who were compared to 40 controls. Endothelial dysfunction was assessed by measurement of flow-mediated dilatation (FMD) and glyceryl trinitrate dilatation (NMD) of the brachial artery. ADMA (micromol/L) was analyzed by ELISA. Results: FMD in patients with APS was significantly lower than that of the controls (p < 0.001), with no difference between the PAPS and the SAPS groups. ADMA and hsCRP concentrations were significantly higher in the patient cohort than in the control group (p < 0.001, p = 0.006, respectively), as was the case with the SAPS group as compared to the PAPS group (p < 0.001, p = 0.022, respectively). FMD impairment correlated to ADMA (ρ 0.472, p < 0.001) and to hsCRP (ρ 0.181, p = 0.033). In the regression model, the ADMA concentration confirmed the strength of its association (B 0.518, SE 0.183, Wald 8.041, p = 0.005, Exp(B) 1.679, 95% CI 1.174−2.402) to FMD impairment. The synergistic probability model of ADMA and hsCRP caused FMD impairment when the positivity of β2GPIIgG was added. ADMA may be used as a simple and low-cost tool for verifying the presence of endothelial dysfunction in APS patients. According to the results of the study, we could presume that hsCRP, together with aPL, has a preparatory effect on the endothelium in causing endothelial dysfunction.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9603922PMC
http://dx.doi.org/10.3390/ijms232012309DOI Listing

Publication Analysis

Top Keywords

endothelial dysfunction
20
aps patients
12
fmd impairment
12
asymmetric dimethylarginine
8
dysfunction aps
8
adma hscrp
8
group 0001
8
model adma
8
adma
7
aps
6

Similar Publications

Cerebrovascular protective functions of amyloid precursor protein: Progress and therapeutic prospects.

Pharmacol Ther

September 2025

Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, MN 55902, USA; Department of Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55902, USA.

Under physiological conditions, amyloid precursor protein (APP) is critically important for normal brain development, neurogenesis, neuronal survival, and synaptic signaling. Dyshomeostasis of APP increases deposition and accumulation of amyloid β (Aβ) in the brain parenchyma and cerebral blood vessels thereby leading to development of Alzheimer's disease and cerebral amyloid angiopathy. In this review, we critically examine existing literature supporting the concept that endothelial APP performs important vascular protective functions in the brain.

View Article and Find Full Text PDF

Light-emitting diode-derived blue light overexposure accelerates corneal endothelial cell aging by inducing abnormal ROS accumulation.

J Photochem Photobiol B

September 2025

The First Affiliated Hospital, Department of Ophthalmology, Hengyang Medical school, University of South China, Hengyang, Hunan 421001, China; Xiamen University Affiliated Xiamen Eye Center, Fujian Provincial Key Laboratory of Ophthalmology and Visual Science, Fujian Engineering and Research Center

Blue light, defined as short-wavelength visible light ranging from 400 to 500 nm, is recognized for its high energy within the visible light spectrum. The prevalent use of light-emitting diodes (LEDs) has significantly increased exposure to blue light. Corneal endothelial cells (CECs) playing a crucial role in maintaining corneal transparency to get clear visual field.

View Article and Find Full Text PDF

Endothelial Dysfunction and Therapeutic Advances in Chronic Kidney Disease.

Diabetes Metab Res Rev

September 2025

Department of Nephrology, Daping Hospital, Army Medical University, Chongqing, China.

Chronic kidney disease (CKD) substantially increases cardiovascular risk, with endothelial dysfunction as its central pathological mechanism. This review summarises the molecular regulatory mechanisms underlying endothelial dysfunction in CKD and highlights recent advances in treatment strategies. The pathophysiology of endothelial injuries involves a complex network of multiple factors and mechanisms, including oxidative stress, inflammation, glycocalyx damage, ischaemia, hypoxia, cellular senescence and endothelial-mesenchymal transition (EndMT).

View Article and Find Full Text PDF

Protocol for live-cell calcium imaging of human lung microvascular endothelial vessel-on-a-chip model.

STAR Protoc

September 2025

Division of Pulmonary Medicine and Critical Care, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Department of Systems Biology and Physiology, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA; Department of Pulmonary Medicine, Cincinnati Children's Hospital Medical C

Calcium signaling is crucial for endothelial cell homeostasis. Alterations in intracellular calcium levels due to shear stress are linked to vascular dysfunction and diseases. Here, we present a protocol to perform live calcium imaging by using a live calcium indicator on human lung endothelial cells subjected to shear stress in a commercially available microfluidic device (Ibidi Luer VI).

View Article and Find Full Text PDF

Unifying Vascular Injury and Neurodegeneration: A Mechanistic Continuum in Cerebral Small Vessel Disease and Dementia.

Eur J Neurosci

September 2025

Global Health Neurology Lab, Sydney, New South Wales, Australia.

Cerebral small vessel disease (CSVD) is a major yet underappreciated driver of cognitive impairment and dementia, contributing to nearly half of all cases. Emerging evidence indicates that CSVD is not merely a coexisting vascular condition but an active amplifier of neurodegeneration, operating through a self-perpetuating cascade of microvascular injury, blood-brain barrier (BBB) breakdown, and glymphatic system dysfunction. In this hypothesis-driven review, we propose the Integrated Vascular-Neurodegenerative Continuum, a mechanistic model in which vascular pathology triggers and accelerates neurodegeneration via intersecting pathways, including chronic cerebral hypoperfusion, oxidative stress, and APOE ε4-associated endothelial vulnerability.

View Article and Find Full Text PDF