Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Endothelin-1 (ET-1) contributes to senescence and phenotypic changes in brain pericytes in diabetes-mimicking conditions.

Clinical science (London, England : 1979) - 21 Aug 2024

Edgerton-Fulton Mia, Abdul Yasir, Jamil Sarah, Ergul Adviye

Abstract excerpt

Diabetes mediates endothelial dysfunction and increases the risk of Alzheimer's disease and related dementias. Diabetes also dysregulates the ET system. ET-1-mediated constriction of brain microvascular pericytes (BMVPCs) has been shown to contribute to brain hypoperfusion. Cellular senescence, a process that arrests the proliferation of harmful cells and instigates phenotypical changes and proinflammatory...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Brain
Share to Cells, Cultured
Share to Cellular Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Diabetes Mellitus

Share to Endothelin-1

Share to Pericytes

Share to Phenotype

Share to Receptor, Endothelin A

Source

Open in PubMed Open full text

Identifiers

PMID: 39106080
DOI: 10.1042/CS20240328
PMCID: PMC12859822

Genes

IGFBP7

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Endothelin-1 (ET-1) contributes to senescence and phenotypic changes in brain pericytes in diabetes-mimicking conditions.PMID 39106080Read ↗

Endothelial Senescence and Its Impact on Angiogenesis in Alzheimer’s DiseaseSemantic proximity Read ↗

Cellular senescence and the blood–brain barrier: Implications for aging and age-related diseasesSemantic proximity Read ↗

Endothelial Senescence and the Chronic Vascular Diseases: Challenges and Therapeutic Opportunities in AtherosclerosisSemantic proximity Read ↗

Oxidative Stress, Neuroinflammation, and Microvascular Damage in Neurodegenerative Diseases: Mechanistic Insights and Therapeutic ApproachesSemantic proximity Read ↗

Vascular ageing and endothelial cell senescence: Molecular mechanisms of physiology and diseasesSemantic proximity Read ↗

Endothelial Progenitor Cells and Vascular Alterations in Alzheimer’s DiseaseSemantic proximity Read ↗

Hypoxia-Inducible Factor-1α: The Master Regulator of Endothelial Cell Senescence in Vascular AgingSemantic proximity Read ↗

Vascular Aging and Atherosclerosis: A Perspective on AgingSemantic proximity Read ↗

Pharmacologically reversible zonation-dependent endothelial cell transcriptomic changes with neurodegenerative disease associations in the aged brainSemantic proximity Read ↗

Dysfunctional vascular smooth muscle cells mediate early and late-stage neuroinflammation and Tau hyperphosphorylationSemantic proximity Read ↗

Long term high glucose exposure induces premature senescence in retinal endothelial cellsSemantic proximity Read ↗

Delay of endothelial cell senescence protects cerebral barrier against age-related dysfunction: role of senolytics and senomorphicsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.