ArticleScience translational medicine2019
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
Article in Science translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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Who cites it
36 citing papers in PubMed, 58 citations in OpenAlex.
- Misregulation of T-box transcription factors drives BNP-NPR1 signalling underlying chronic itch.Nature communications · 2026Article
- Discovery of an Adaptive Neuroimmune Response Driving Itch and Fast Tick Removal with Implications for Preventing Pathogen Transmission.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Substance P and somatostatin neurons limit facial itch by recruiting distinct nociceptive circuits in the brainstem.Communications biology · 2026Article
- Discovery of an Adaptive Neuroimmune Response Driving Itch and Fast Tick Removal with Implications for Preventing Pathogen Transmission.bioRxiv : the preprint server for biology · 2025Article
- Distinct Neural Mechanisms in the Propagation of Itch in the Face and Body.Research square · 2025Article
- An atlas of neuropathic pain-associated molecular pathological characteristics in the mouse spinal cord.Communications biology · 2025Article
- The neuroscience of itch in relation to transdiagnostic psychological approaches.Scientific reports · 2024Article
- Identification and Management of CKD-Associated Pruritus: Current Insights.International journal of nephrology and renovascular disease · 2024Review
- Article
- qHTSWaterfall: 3-dimensional visualization software for quantitative high-throughput screening (qHTS) data.Journal of cheminformatics · 2023Article
- Neurotrophins: Neuroimmune Interactions in Human Atopic Diseases.International journal of molecular sciences · 2023Review
- Reference compounds for characterizing cellular injury in high-content cellular morphology assays.Nature communications · 2023Article
- In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.Disease models & mechanisms · 2023Article
- Pathogenesis and Treatment of Pruritus Associated with Chronic Kidney Disease and Cholestasis.International journal of molecular sciences · 2023Review
- Paracatalytic induction: Subverting specificity in hedgehog protein autoprocessing with small molecules.Methods in enzymology · 2023Article
- Critical Players and Therapeutic Targets in Chronic Itch.International journal of molecular sciences · 2022Review
- The translational revolution of itch.Neuron · 2022Review
- GPR15L is an epithelial inflammation-derived pruritogen.Science advances · 2022Article
- Predicting Prenatal Developmental Toxicity Based On the Combination of Chemical Structures and Biological Data.Environmental science & technology · 2022Article
- Specific β-Defensins Stimulate Pruritus through Activation of Sensory Neurons.The Journal of investigative dermatology · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
There is a major clinical need for new therapies for the treatment of chronic itch. Many of the molecular components involved in itch neurotransmission are known, including the neuropeptide NPPB, a transmitter required for normal itch responses to multiple pruritogens in mice. Here, we investigated the potential for a novel strategy for the treatment of itch that involves the inhibition of the NPPB receptor NPR1 (natriuretic peptide receptor 1). Because there are no available effective human NPR1 (hNPR1) antagonists, we performed a high-throughput cell-based screen and identified 15 small-molecule hNPR1 inhibitors. Using in vitro assays, we demonstrated that these compounds specifically inhibit hNPR1 and murine NPR1 (mNPR1). In vivo, NPR1 antagonism attenuated behavioral responses to both acute itch- and chronic itch-challenged mice. Together, our results suggest that inhibiting NPR1 might be an effective strategy for treating acute and chronic itch.
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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.