ArticleScientific reports2025
Muscarinic acetylcholine receptor 3 localized to primary endothelial cilia regulates blood pressure and cognition.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Endothelial dysfunction: A central mechanism linking autosomal dominant polycystic kidney disease and intracranial aneurysms (Review).International journal of molecular medicine · 2026Review
- Neurotransmitter Dysregulation in Parkinson's Disease: Pathophysiological Insights and Therapeutic Perspectives.ACS chemical neuroscience · 2026Review
- Blockers of Acetylcholine Receptors Affect the Hypotensive Effect of the Central Loop Fragment of the WTX Toxin.Doklady. Biochemistry and biophysics · 2026Article
- A Transcriptional Atlas of Endothelial Cell Zonation Along the Pulmonary Vascular Tree.bioRxiv : the preprint server for biology · 2026Article
- Primary Cilia and Cardiovascular Risk Factors in Alzheimer's Disease.Brain sciences · 2025Review
- Ciliary G-Protein Coupled Receptor Signaling in Polycystic Kidney Disease.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
We previously demonstrated that the inability of primary endothelial cilia to sense fluid shear stress can lead to nitric oxide (NO) deficiency and cause hypertension (HTN). Decreased biosynthesis of NO contributes to cerebral amyloid angiopathy in Alzheimer's disease (AD) patients through increased deposition of amyloid beta (Aβ). However, the molecular mechanisms underlying the pathogenesis of HTN and AD are incompletely understood. The objective of this study was to examine the pathophysiological roles of vascular primary cilia and muscarinic acetylcholine receptor 3 (CHRM3) in HTN and AD. We discovered, for the first time, that CHRM3 was localized to primary cilia of endothelial and cerebrovascular cells, and that CHRM3 expression was downregulated in cilialess cells. Moreover, CHRM3 activation enhanced cilia length and sensory function in terms of eNOS activation. To further examine the role of vascular CHRM3 in vivo, we showed that endothelial CHRM3 knockout was associated with increased BP and attenuated acetylcholine-mediated vascular relaxation. In addition, endothelial CHRM3 knockout resulted in altered fear behavior. This demonstrates the physiological significance of endothelial CHRM3 signaling and primary cilia-derived NO production as an important mechanism in the control of BP and cognition.
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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.