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Updated: Jul 25, 2025

Proteomics to Identify Proteins Interacting with P2X2 Ligand-Gated Cation Channels
Published on: May 18, 2009
Role and therapeutic target of P2X2/3 receptors in visceral pain
Hong-Mei Luo1, Jia-Rong Ye2, Fan-Qin Pu1
1Department of Rheumatology, The Affiliated Hospital of Jiangxi University of Chinese Medicine, Nanchang City, Jiangxi province 343000, China.
Abstract:
Visceral pain (VP) is caused by internal organ disease. VP is involved in nerve conduction and related signaling molecules, but its specific pathogenesis has not yet been fully elucidated. Currently, there are no effective methods for treating VP. The role of P2X2/3 in VP has progressed. After visceral organs are subjected to noxious stimulation, cells release ATP, activate P2X2/3, enhance the sensitivity of peripheral receptors and the plasticity of neurons, enhance sensory information transmission, sensitize the central nervous system, and play an important role in the development of VP. However, antagonists possess the pharmacological effect of relieving pain. Therefore, in this review, we summarize the biological functions of P2X2/3 and discuss the intrinsic link between P2X2/3 and VP. Moreover, we focus on the pharmacological effects of P2X2/3 antagonists on VP therapy and provide a theoretical basis for its targeted therapy.
Insights
The P2X2/3 receptor plays a key role in visceral pain (VP) development by enhancing nerve sensitivity and transmission. P2X2/3 antagonists show promise for effective VP targeted therapy.
Area of Science:
- Neuroscience
- Pharmacology
- Pain Research
Background:
- Visceral pain (VP) pathogenesis is not fully understood, with limited effective treatments.
- The P2X2/3 receptor's role in VP is an emerging area of research.
- ATP release and P2X2/3 activation are implicated in visceral hypersensitivity.
Purpose of the Study:
- To review the biological functions of the P2X2/3 receptor.
- To elucidate the link between P2X2/3 and visceral pain.
- To discuss the therapeutic potential of P2X2/3 antagonists for VP.
Main Methods:
- Literature review focusing on P2X2/3 receptor function and VP.
- Analysis of signaling pathways involving ATP and P2X2/3 in visceral nociception.
- Evaluation of pharmacological data on P2X2/3 antagonists in VP models.
Main Results:
- P2X2/3 activation enhances peripheral receptor sensitivity and neuronal plasticity.
- P2X2/3 signaling contributes to central nervous system sensitization in VP.
- P2X2/3 antagonists demonstrate pain-relieving effects.
Conclusions:
- P2X2/3 is a significant mediator in the development of visceral pain.
- Targeting P2X2/3 with antagonists offers a promising therapeutic strategy for VP.
- Further research into P2X2/3 antagonists can provide a basis for novel VP treatments.
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