Neuropathic pain (NP), as a common and refractory chronic pain, is caused by damage or diseases of the somatosensory system. The clinical manifestations are mainly spontaneous pain and induced pain, which bring great distress to patients. The mechanisms involved in NP have not been fully elucidated, and it has been widely accepted that peripheral and central sensitization after a nerve injury play critical roles in induction and maintenance of NP. Peripheral sensitization is mainly related to ectopic discharge induced by sympathetic sprouting associated with changes in related ion channels, peripheral inflammatory responses, transcriptional disorders of genes related to non-coding RNAs, and changes in pain signal transduction, while central sensitization is closely related to inflammatory responses, abnormal activation of glial cells and dysfunction of central nervous system. Herein, the mechanisms underlying peripheral and central sensitiza-tion resulted from nerve injuries were reviewed, hoping to provide new ideas for basic research on NP and its treatment.