Fluorescent nanocarriers targeting VCAM-1 for early detection of senescent endothelial cells

VCAM-1 as a Biomarker of Endothelial Function among HIV-Infected Patients Receiving and Not Receiving Antiretroviral Therapy

“…Moreover, alpha D beta 2 binds to VCAM-1 and can also support lymphoid cell adhesion to VCAM-1 [47]. One study developed the theranostic nanocarriers decorated with VCAM-1 antibodies that seem to localize the endothelial senescence and prevent pro-senescent endothelial responses [48]. Nutraceuticals, which are dietary supplements, are currently gaining attention due to their therapeutic potential [49].…”

Acute effects of cigarette smoke on Endothelial Nitric Oxide synthase, vascular cell adhesion molecule 1 and aortic intima media thickness

“…In his previous research, soluble VCAM-1 levels were increased in smokers' serum but not significantly when compared to non-smokers' serum. 23 Increase of VCAM-1 expression is a multifactorial process, smoking could not increase VCAM-1 independently without other risk factors such as dyslipidemia. Mu et al (2015) had proven this hypothesis by examining VCAM-1 expression in aortic tissue of dyslipidemia patients.…”

Targeted Imaging in Atherosclerosis

“…Dysfunctional ECs enable biomacromolecules such as low-density lipoprotein to penetrate and accumulate into the vascular intima, secrete a variety of growth factors, adhesion molecules, and chemokines, and promote the occurrence and development of atherosclerosis . Moreover, overexpressed adhesion molecules on the surface of activated ECs, such as VCAM-1, ICAM-1, E-selectins, and P-selectins, have been proposed as potential targets for imaging the atherosclerosis. For example, Mi et al prepared P-selectin specific complex nanoparticles by the electrostatic complexation of fucoidan polymer with thermolysin-hydrolyzed protamine peptide loaded a the magnetic resonance contrast agent for accurate imaging of inflamed ECs .…”

“…Atherosclerosis (AS), a chronic inflammatory disease that involves many complex processes, including lipid deposition on the blood vessel wall and asymptomatic buildup of plaques, is the main pathological basis of cardiovascular disease. − Endothelial dysfunction, proliferation and migration of vascular smooth muscle cells (VSMCs), and formation of foamy macrophages are the primary factors for the occurrence and development of atherosclerosis. − A variety of risk pathogenic factors (including abnormal blood flow shear stress, obesity, hyperlipidemia, hypertension, tobacco smoke, alcohol, etc.) repeatedly stimulate endothelial cells (ECs) for a long time, resulting in dysfunction of ECs involved in abnormal secretion functions and increased endothelial permeability. , Furthermore, ECs secrete a large number of inflammatory factors and chemokines, recruit monocytes from circulating blood to the location of the endothelial injury, and activate the expression of adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1) , and intracellular adhesion molecule-1 (ICAM-1) . Then these monocytes further migrate, infiltrate, and differentiate into macrophages.…”

“…repeatedly stimulate endothelial cells (ECs) for a long time, resulting in dysfunction of ECs involved in abnormal secretion functions and increased endothelial permeability. 7,8 Furthermore, ECs secrete a large number of inflammatory factors and chemokines, recruit monocytes from circulating blood to the location of the endothelial injury, and activate the expression of adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1) 9,10 and intracellular adhesion molecule-1 (ICAM-1). 11 Then these monocytes further migrate, infiltrate, and differentiate into macrophages.…”