• Xinxin Wang, Jiajun Ju, Yafei Xie, and Lihua Hang.
• Department of Anesthesiology, Kunshan Hospital Affiliated to Jiangsu University, Suzhou, 215300, China. Electronic address: 1272355453@qq.com.
• Neuroscience. 2024 Nov 1; 559: 199208199-208.

AbstractNeurological disorders and pain are prevalent clinical issues that severely impact patients' quality of life and daily functioning. With the advancing exploration of these disease mechanisms, G protein-coupled receptor 37 (GPR37) has emerged as a critical protein, garnering widespread attention in the scientific community. As a member of the G protein-coupled receptor family, GPR37 features a seven-transmembrane helix structure and is widely expressed in various brain regions, including the substantia nigra and striatum. In addition to neurons, GPR37 is also detected in immune cells within the nervous system, indicating its potential role in neuron-immune cell interactions. Research has shown that the expression level of GPR37 in neurological disorders can affect neuron survival, cellular signaling, and overall neurological health. Abnormal expression of GPR37 is often associated with disease progression and symptom exacerbation in neurological disorders such as Parkinson's disease and stroke. In the context of pain, GPR37 alleviates pain and inflammatory responses by regulating the phagocytic activity and polarization state of macrophages. This article aims to delve into the mechanistic roles of GPR37 in neurological disorders and pain. Through a comprehensive literature review, we summarize the latest research on GPR37's involvement in neurological diseases and pain, highlighting its critical roles in neural signaling, inflammatory responses, and neuroprotection. This understanding expands the comprehension of GPR37's biological functions and provides new perspectives for improving the clinical outcomes of patients with neurological disorders and pain.Copyright © 2024 International Brain Research Organization (IBRO). Published by Elsevier Inc. All rights reserved.

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