ReviewFrontiers in physiology2022
Cerebral Microvascular Senescence and Inflammation in Diabetes.
Review in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Translational Barriers and Optimization Strategies for Remote Ischemic Conditioning to Enhance Stroke Cerebroprotection.Biomolecules · 2026Review
- Cellular Senescence in Neurodegeneration: From Cell Types to Therapeutic Opportunities.Biomedicines · 2026Review
- Metabolomic etiological insights into six diabetic complications: a large scale Mendelian randomization atlas with colocalization validation.Acta diabetologica · 2026Article
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- Hypoglycemia aggravates cognitive degeneration by activating endothelial ZBP1-mediated PANoptosis in type 2 diabetic mice.Frontiers in pharmacology · 2026Article
- A Review of Emerging Biomarkers Connecting Diabetes and Ischemic Stroke: Implications for Early Detection and Risk Stratification.Journal of diabetes research · 2026Review
- Risk Factors, Pathological Changes, and Potential Treatment of Diabetes-Associated Cognitive Dysfunction.Journal of diabetes · 2025Review
- The role of VEGF in vascular dementia: impact of aging and cellular senescence.Biogerontology · 2025Review
- Combination treatment with cilostazol and isosorbide mononitrate attenuates microemboli-mediated vascular cognitive impairment and improves imaging and plasma biomarkers in diabetic rats.Experimental neurology · 2025Article
- Zi Shen Wan Fang repaired blood-brain barrier integrity in diabetic cognitive impairment mice via preventing cerebrovascular cells senescence.Chinese medicine · 2024Article
- Endothelin-1 (ET-1) contributes to senescence and phenotypic changes in brain pericytes in diabetes-mimicking conditions.Clinical science (London, England : 1979) · 2024Article
- Aging insights from heterochronic parabiosis models.npj aging · 2024Review
- An update on chronic complications of diabetes mellitus: from molecular mechanisms to therapeutic strategies with a focus on metabolic memory.Molecular medicine (Cambridge, Mass.) · 2024Review
- The pharmacology and therapeutic role of cannabidiol in diabetes.Exploration (Beijing, China) · 2023Article
- Review
- Impact of Dietary Fiber on Inflammation and Insulin Resistance in Older Patients: A Narrative Review.Nutrients · 2023Review
- Cellular senescence and the blood-brain barrier: Implications for aging and age-related diseases.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Neurovascular coupling in patients with type 2 diabetes mellitus.Frontiers in aging neuroscience · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Stress-induced premature senescence can contribute to the accelerated metabolic aging process in diabetes. Progressive accumulation of senescent cells in the brain, especially those displaying the harmful inflammatory senescence-associated secretory phenotype (SASP), may lead to cognitive impairment linked with metabolic disturbances. In this context, the senescence within the neurovascular unit (NVU) should be studied as much as in the neurons as emerging evidence shows that neurogliovascular communication is critical for brain health. It is also known that cerebrovascular dysfunction and decreased cerebral blood flow (CBF) precede the occurrence of neuronal pathologies and overt cognitive impairment. Various studies have shown that endothelial cells, the major component of the NVU, acquire a senescent phenotype via various molecular mediators and pathways upon exposure to high glucose and other conditions mimicking metabolic disturbances. In addition, senescence in the other cells that are part of the NVU, like pericytes and vascular smooth cells, was also triggered upon exposure to diabetic conditions. The senescence within the NVU may compromise functional and trophic coupling among glial, vascular, and neuronal cells and the resulting SASP may contribute to the chronic neurovascular inflammation observed in Alzheimer's Disease and Related Dementias (ADRD). The link between diabetes-mediated cerebral microvascular dysfunction, NVU senescence, inflammation, and cognitive impairment must be widely studied to design therapeutic strategies.
Indexed as
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.