Extracellular signal-regulated kinases (ERK) 1 and 2 as a key molecule in pain research.

Pain can be divided into nociceptive, inflammatory, and neuropathic pain. It is important to understanding the molecular mechanism of pain signaling in the development of pain relief therapies. Twenty years ago, extracellular signal-regulated kinases (ERK) 1 and 2, which are members of the mitogen-activated protein kinase superfamily, were identified as molecules activated in neurons by the exposure of peripheral tissues to noxious stimuli. Further studies have revealed that peripheral nerve injury induces ERK activation in glial cells, sensory neurons, and second-order neurons, albeit at different time points. Moreover, inhibition of ERK suppresses pathological pain in animals with peripheral nerve injury. Therefore, ERK is currently recognized as an important molecule in pain signaling and a potential novel target for pain treatment. This review introduces recent advances in revealing the regulation of ERK in pain research.