ReviewFrontiers in cellular neuroscience2025
Role and regulatory mechanism of GPR37 in neurological diseases.
Review in Frontiers in cellular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed.
- A Sesquiterpenoid fromInternational journal of molecular sciences · 2026Article
- Decoding GPCR signaling in living cells to advance early therapeutic discovery for neurological disorders.Frontiers in molecular neuroscience · 2026Review
- Oligodendrocyte dysfunction in neurodegenerative diseases: pathological features, underlying mechanisms and therapeutic targeting.Frontiers in aging neuroscience · 2026Review
- Macrophages: their role in immunity and their relationship with fatty acids in health and disease.Frontiers in immunology · 2025Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
G protein-coupled receptor 37 is an orphan Class A GPCR predominantly expressed in the central nervous system (CNS), implicated in diverse physiological and pathological processes. This review summarizes current advances in the structural and functional understanding of GPR37, including its genomic localization, receptor architecture, endogenous ligands, and downstream signaling pathways. Emphasis is placed on its cell-type-specific expression across neurons, astrocytes, microglia, and oligodendrocytes, and how this expression dynamically shifts under pathological contexts such as Parkinson's disease, stroke, and demyelinating disorders. GPR37 modulates neuroinflammatory responses, apoptosis, and oxidative stress through context-dependent mechanisms shaped by its ligands, including prosaposin, neuroprotectin D1, and osteocalcin. Additionally, GPR37 dysfunction-especially via receptor misfolding and ER stress-contributes to neuronal vulnerability. We further discuss its emerging role as a pharmacological target and potential biomarker in CNS disorders. By integrating findings across molecular, cellular, and disease models, we propose a context-dependent framework positioning GPR37 as a multifunctional regulator and therapeutic candidate in neurodegeneration.
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Registered trials
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