ArticleProceedings of the National Academy of Sciences of the United States of America2007
Serum response factor and myocardin mediate arterial hypercontractility and cerebral blood flow dysregulation in Alzheimer's phenotype.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.
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Who cites it
113 citing papers in PubMed, 208 citations in OpenAlex.
- Gene-Environment Interactions for Alzheimer's Disease Pathology in Cognitively Normal Adults: The CABLE Study.European journal of neurology · 2026Article
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
- Neurovascular phase coherence is altered in Alzheimer's disease.Brain communications · 2025Article
- Umbelliferone as an effective component of Rhodiola for protecting the cerebral microvascular endothelial barrier in cSVD.Frontiers in pharmacology · 2025Article
- Targeting serum response factor (SRF) deactivates ΔFosB and mitigates Levodopa-induced dyskinesia in a mouse model of Parkinson's disease.Gene therapy · 2024Article
- Article
- Human iPSC-derived pericyte-like cells carrying APP Swedish mutation overproduce beta-amyloid and induce cerebral amyloid angiopathy-like changes.Fluids and barriers of the CNS · 2024Article
- Elevated cerebral blood flow proxy with increased beta-amyloid burden in Alzheimer's disease preclinical phase evaluated by dual-phaseScientific reports · 2024Article
- Amyloid-β: A potential mediator of aging-related vascular pathologies.Vascular pharmacology · 2023Review
- Mural Serum Response Factor (SRF) Deficiency Provides Insights into Retinal Vascular Functionality and Development.International journal of molecular sciences · 2023Article
- SRF deletion results in earlier disease onset in a mouse model of amyotrophic lateral sclerosis.JCI insight · 2023Article
- Vascular contributions to Alzheimer's disease.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Could Mid- to Late-Onset Glaucoma Be Associated with an Increased Risk of Incident Dementia? A Nationwide Retrospective Cohort Study.Journal of personalized medicine · 2023Article
- Microglia-Mediated Neurovascular Unit Dysfunction in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- Long-Term Repeatable In Vivo Monitoring of Amyloid-β Plaques and Vessels in Alzheimer's Disease Mouse Model with Combined TPEF/CARS Microscopy.Biomedicines · 2022Article
- The relationship between amyloid-beta and brain capillary endothelial cells in Alzheimer's disease.Neural regeneration research · 2022Review
- Fasting-mimicking diet cycles reduce neuroinflammation to attenuate cognitive decline in Alzheimer's models.Cell reports · 2022Article
- SRF in Neurochemistry: Overview of Recent Advances in Research on the Nervous System.Neurochemical research · 2022Review
- SRF: a seriously responsible factor in cardiac development and disease.Journal of biomedical science · 2022Review
- Old blood from heterochronic parabionts accelerates vascular aging in young mice: transcriptomic signature of pathologic smooth muscle remodeling.GeroScience · 2022Article
53 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 6 institutions in 4 countries.
Funding
Abstract
Cerebral angiopathy contributes to cognitive decline and dementia in Alzheimer's disease (AD) through cerebral blood flow (CBF) reductions and dysregulation. We report vascular smooth muscle cells (VSMC) in small pial and intracerebral arteries, which are critical for CBF regulation, express in AD high levels of serum response factor (SRF) and myocardin (MYOCD), two interacting transcription factors that orchestrate a VSMC-differentiated phenotype. Consistent with this finding, AD VSMC overexpressed several SRF-MYOCD-regulated contractile proteins and exhibited a hypercontractile phenotype. MYOCD overexpression in control human cerebral VSMC induced an AD-like hypercontractile phenotype and diminished both endothelial-dependent and -independent relaxation in the mouse aorta ex vivo. In contrast, silencing SRF normalized contractile protein content and reversed a hypercontractile phenotype in AD VSMC. MYOCD in vivo gene transfer to mouse pial arteries increased contractile protein content and diminished CBF responses produced by brain activation in wild-type mice and in two AD models, the Dutch/Iowa/Swedish triple mutant human amyloid beta-peptide (Abeta)-precursor protein (APP)- expressing mice and APPsw(+/-) mice. Silencing Srf had the opposite effect. Expression of SRF did not change in VSMC subjected to Alzheimer's neurotoxin, Abeta. Thus, SRF-MYOCD overexpression in small cerebral arteries appears to initiate independently of Abeta a pathogenic pathway mediating arterial hypercontractility and CBF dysregulation, which are associated with Alzheimer's dementia.
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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 OpenQuestion graph.