ArticlePloS one2010
Amyloid-β inhibits No-cGMP signaling in a CD36- and CD47-dependent manner.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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Who cites it
37 citing papers in PubMed, 51 citations in OpenAlex.
- Suppression of neuronal eEF2K alleviates cognitive deficits and apathy-like behavior in APP/PS1 AD model mice.Research square · 2026Article
- Deciphering the role of CD47 in cancer immunotherapy.Journal of advanced research · 2024Review
- Tolerating CD47.Clinical and translational medicine · 2024Review
- Dysregulated C1q and CD47 in the aging monkey brain: association with myelin damage, microglia reactivity, and cognitive decline.Frontiers in immunology · 2024Article
- The TSP1-CD47-SIRPα interactome: an immune triangle for the checkpoint era.Cancer immunology, immunotherapy : CII · 2023Review
- The Reversal Characteristics of GABAergic Neurons: A Neurovascular Model.Journal of biomechanical engineering · 2023Article
- The Interplay between cGMP and Calcium Signaling in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Transforming growth factor-β1/Thrombospondin-1/CD47 axis mediates dysfunction in CD34European journal of pharmacology · 2022Article
- Single-synapse analyses of Alzheimer's disease implicate pathologic tau, DJ1, CD47, and ApoE.Science advances · 2021Article
- CD47 and thrombospondin-1 regulation of mitochondria, metabolism, and diabetes.American journal of physiology. Cell physiology · 2021Review
- Role of JAK/STAT in the Neuroinflammation and its Association with Neurological Disorders.Annals of neurosciences · 2021Review
- CD47 in the Brain and Neurodegeneration: An Update on the Role in Neuroinflammatory Pathways.Molecules (Basel, Switzerland) · 2021Review
- Soluble Receptors Affecting Stroke Outcomes: Potential Biomarkers and Therapeutic Tools.International journal of molecular sciences · 2021Review
- CD47 (Cluster of Differentiation 47).Atlas of genetics and cytogenetics in oncology and haematology · 2021Article
- Inflammation, Nitro-Oxidative Stress, Impaired Autophagy, and Insulin Resistance as a Mechanistic Convergence Between Arterial Stiffness and Alzheimer's Disease.Frontiers in molecular biosciences · 2021Review
- Elevated circulating amyloid concentrations in obesity and diabetes promote vascular dysfunction.The Journal of clinical investigation · 2020Article
- Role of CD47 in Hematological Malignancies.Journal of hematology & oncology · 2020Review
- Thrombospondin-1 in maladaptive aging responses: a concept whose time has come.American journal of physiology. Cell physiology · 2020Review
- The Alzheimer's Disease Amyloid-Beta Hypothesis in Cardiovascular Aging and Disease: JACC Focus Seminar.Journal of the American College of Cardiology · 2020Review
- THBS1/CD47 Modulates the Interaction of γ-Catenin With E-Cadherin and Participates in Epithelial-Mesenchymal Transformation in Lipid Nephrotoxicity.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Amyloid-β interacts with two cell surface receptors, CD36 and CD47, through which the matricellular protein thrombospondin-1 inhibits soluble guanylate cyclase activation. Here we examine whether amyloid-β shares this inhibitory activity. Amyloid-β inhibited both drug and nitric oxide-mediated activation of soluble guanylate cyclase in several cell types. Known cGMP-dependent functional responses to nitric oxide in platelets and vascular smooth muscle cells were correspondingly inhibited by amyloid-β. Functional interaction of amyloid-β with the scavenger receptor CD36 was indicated by inhibition of free fatty acid uptake via this receptor. Both soluble oligomer and fibrillar forms of amyloid-β were active. In contrast, amyloid-β did not compete with the known ligand SIRPα for binding to CD47. However, both receptors were necessary for amyloid-β to inhibit cGMP accumulation. These data suggest that amyloid-β interaction with CD36 induces a CD47-dependent signal that inhibits soluble guanylate cyclase activation. Combined with the pleiotropic effects of inhibiting free fatty acid transport via CD36, these data provides a molecular mechanism through which amyloid-β can contribute to the nitric oxide signaling deficiencies associated with Alzheimer's disease.
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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.