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World J Anesthesiol. Mar 27, 2014; 3(1): 71-81
Published online Mar 27, 2014. doi: 10.5313/wja.v3.i1.71
Published online Mar 27, 2014. doi: 10.5313/wja.v3.i1.71
Molecular mechanism of inflammatory pain
Yeu-Shiuan Su, Wei-Hsin Sun, Department of Life Sciences, National Central University, Jhongli 32054, Taiwan
Chih-Cheng Chen, Institute of Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan
Chih-Cheng Chen, Taiwan Mouse Clinic-National Phenotyping and Drug Testing Center, Academia Sinica, Taipei 115, Taiwan
Author contributions: Su YS and Sun WH contributed equally to this work, collected literatures, and wrote the manuscript; Chen CC designed the scope of the minireview and wrote the manuscript.
Correspondence to: Chih-Cheng Chen, PhD, Institute of Biomedical Sciences, Academia Sinica, 128 Academia Road, Section 2, Taipei 115, Taiwan. chih@ibms.sinica.edu.tw
Telephone: +886-2-26523917 Fax: +886-2-27829224
Received: June 29, 2013
Revised: September 27, 2013
Accepted: November 1, 2013
Published online: March 27, 2014
Processing time: 255 Days and 11.3 Hours
Revised: September 27, 2013
Accepted: November 1, 2013
Published online: March 27, 2014
Processing time: 255 Days and 11.3 Hours
Core Tip
Core tip: Tissue acidosis that occurs during inflammation is central to the development and maintenance of chronic pain. Recent studies have revealed a variety of proton-sensing ion channels (e.g., acid-sensing ion channels, transient receptor potential V1) and G-protein-coupled receptors (e.g., G2 accumulation 2A, G-protein-coupled receptor 4, ovarian cancer G-protein-coupled receptor, T-cell death-associated gene 8) responsible for acid-induced pain. These cell-surface membrane proteins are promising therapeutic targets for the development of new analgesic drugs for chronic inflammatory pain.