ArticleNeurobiology of aging2015
Effect of IP3R3 and NPY on age-related declines in olfactory stem cell proliferation.
Article in Neurobiology of aging, 2015. 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.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- FAK inhibition following acute olfactory epithelial inflammation promotes neurogenesis and functional recovery through stem cell CNTF.Stem cells (Dayton, Ohio) · 2026Article
- Stem cell CNTF promotes olfactory epithelial neuroregeneration and functional recovery following injury.Stem cells (Dayton, Ohio) · 2025Article
- Role and Mechanism of Olfactory Stem Cells in the Treatment of Olfactory Disorders.Stem cells international · 2025Review
- Article
- Sensory Transduction in Photoreceptors and Olfactory Sensory Neurons: Common Features and Distinct Characteristics.Frontiers in cellular neuroscience · 2021Review
- Inhibition of focal adhesion kinase increases adult olfactory stem cell self-renewal and neuroregeneration through ciliary neurotrophic factor.Stem cell research · 2020Article
- Increased Retinoic Acid Catabolism in Olfactory Sensory Neurons Activates Dormant Tissue-Specific Stem Cells and Accelerates Age-Related Metaplasia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- TRPM5-expressing Microvillous Cells Regulate Region-specific Cell Proliferation and Apoptosis During Chemical Exposure.Neuroscience · 2020Article
- Vitronectin mitigates stroke-increased neurogenesis only in female mice and through FAK-regulated IL-6.Experimental neurology · 2020Article
- Age-Related Olfactory Dysfunction: Epidemiology, Pathophysiology, and Clinical Management.Frontiers in aging neuroscience · 2020Review
- Age-Dependent Activation and Neuronal Differentiation of Lgr5+ Basal Cells in Injured Olfactory EpitheliumFrontiers in aging neuroscience · 2020Article
- Vitronectin from brain pericytes promotes adult forebrain neurogenesis by stimulating CNTF.Experimental neurology · 2019Article
- Purinergic Signaling in the Vertebrate Olfactory System.Frontiers in cellular neuroscience · 2019Review
- Inhibition of astrocyte FAK-JNK signaling promotes subventricular zone neurogenesis through CNTF.Glia · 2018Article
- Effects of Neuropeptide Y on Stem Cells and Their Potential Applications in Disease Therapy.Stem cells international · 2017Review
- Ascl3 transcription factor marks a distinct progenitor lineage for non-neuronal support cells in the olfactory epithelium.Scientific reports · 2016Article
- Contribution of Polycomb group proteins to olfactory basal stem cell self-renewal in a novel c-KIT+ culture model and in vivo.Development (Cambridge, England) · 2016Article
- Pathophysiology of Olfactory Disorders and Potential Treatment Strategies.Current otorhinolaryngology reports · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Losing the sense of smell because of aging compromises health and quality of life. In the mouse olfactory epithelium, aging reduces the capacity for tissue homeostasis and regeneration. The microvillous cell subtype that expresses both inositol trisphosphate receptor type 3 (IP3R3) and the neuroproliferative factor neuropeptide Y (NPY) is critical for regulation of homeostasis, yet its role in aging is undefined. We hypothesized that an age-related decline in IP3R3 expression and NPY signaling underlie age-related homeostatic changes and olfactory dysfunction. We found a decrease in IP3R3(+) and NPY(+) microvillous cell numbers and NPY protein and a reduced sensitivity to NPY-mediated proliferation over 24 months. However, in IP3R3-deficient mice, there was no further age-related reduction in cell numbers, proliferation, or olfactory function compared with wild type. The proliferative response was impaired in aged IP3R3-deficient mice when injury was caused by satratoxin G, which induces IP3R3-mediated NPY release, but not by bulbectomy, which does not evoke NPY release. These data identify IP3R3 and NPY signaling as targets for improving recovery following olfactotoxicant exposure.
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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 OpenQuestion graph.