Résumé
Endoplasmic reticulum is one of the most important organelles in maintaining cellular homeo⁃ stasis, mainly involved in intracellular lipid synthesis, protein folding and calcium ion homeostasis. Trau⁃ ma, ischemia and hypoxia and other pathological changes can cause protein folding dysfunction in the en⁃ doplasmic reticulum, triggering endoplasmic reticulum stress (ERS). Spinal cord injury (SCI) is a com⁃ mon traumatic disease with anextremely high disability rate, which seriously affects the quality of life. There is no safe and effective clinical methods so far. Investigations have shown that ERS is one of the important pathological changes leading to cell death and neuronal dysfunction after SCI, and is closely as⁃ sociated with signaling pathways such as apoptosis, autophagy, and inflammation in neurons after SCI; however, the molecular mechanisms between ERS and SCI have not yet been thoroughly investigated. A deeper understanding and exploration of the potential molecular mechanisms associated with ERS and SCI may be the future SCI therapeutics. In this paper, we first summarized the relationship between the chan⁃ ges of ERS⁃related genes and the pathological process of SCI, Then the interrelationships between ERS and the apoptosis, inflammation, and autophagy signaling pathways after SCI were analyzed, starting from the three main modes of regulation, including unfolded protein response (UPR), endoplasmic reticulum⁃ associated degradation (ERAD), and endoplasmic reticulophagy (ER⁃phagy),Finally, we summarize the relevant drugs and application prospects of targeting ERS for SCI in recent years, which may provide a theoretical basis for targeting the ERS pathway for SCI and provide some ideas and insights for the de⁃ velopment of future therapeutic strategies after SCI.