Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10841038PMC
http://dx.doi.org/10.1161/ATVBAHA.123.319514DOI Listing

Publication Analysis

Top Keywords

impairment endothelial
4
endothelial function
4
function cigarette
4
cigarette smoke
4
smoke e-cigarette
4
e-cigarette aerosol
4
aerosol requires
4
requires rage
4
impairment
1
function
1

Similar Publications

Endothelial to mesenchymal transition: a central mechanism in diabetes-induced vascular pathology.

Korean J Physiol Pharmacol

September 2025

Department of Physiology & Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Korea.

Diabetes mellitus is a major global health concern associated with micro-and macrovascular complications. Among the diverse mechanisms that contribute to vascular dysfunction in diabetes, endothelial to mesenchymal transition (EndMT) has emerged as a key pathological process. EndMT involves the loss of endothelial cell characteristics and the acquisition of mesenchymal features, resulting in impaired endothelial function, increased fibrosis, and inflammation.

View Article and Find Full Text PDF

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

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

Background: Endothelial inflammation is involved in cerebral small vessel disease (CSVD) pathogenesis. Vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) are biomarkers of endothelial inflammation.

Aims: This study investigated association of VCAM-1 and ICAM-1 with presence of CSVD and CSVD burden.

View Article and Find Full Text PDF

Intravascular hemolysis (IVH), a pathological process associated with various conditions, triggers inflammatory responses, yet the key molecular drivers of these responses are poorly defined, particularly within the vasculature. To explore the role of NLRP3 inflammasome- and caspase-1-dependent pathways in IVH-induced vascular dysfunction, we used models of acute and chronic IVH, alongside heme stimulation of endothelial cells, thereby isolating this disease mechanism from its etiological causes. IVH induced rapid inflammatory responses in C57BL/6J mice, including IL-1β release within 15 minutes, and NLRP3-dependent caspase-1 activation in circulating leukocytes.

View Article and Find Full Text PDF