HS-1-associated protein X-1 (Hax-1) has been suggested to be expressed in various rodent and human tissues. Accumulating evidence has demonstrated that Hax‑1 exerts an anti‑apoptotic effect in neurological diseases. Furthermore, it has also been reported that Hax‑1 interacts with various apoptosis‑associated proteins, including high temperature-regulated A2 (HtrA2) and caspase‑3. Previous studies have indicated that abnormal expression of Hax‑1 may be associated with the development of the nervous system and with the pathophysiology of neurological diseases, including traumatic brain injury and cerebral ischemia. The present study reported temporal‑spatial patterns of Hax‑1 in rat retina following optic nerve crush (ONC). Using western blotting and double‑immunofluorescence, significant upregulation of Hax‑1 was observed in retinal ganglion cells (RGCs) in the retina following ONC. Increased Hax‑1 expression was demonstrated to be accompanied by upregulation of active‑caspase‑3 and HtrA2 following ONC. In addition, Hax-1 co‑localized with active caspase‑3 and HtrA2 in RGCs following ONC. Terminal deoxynucleotidyl transferase‑mediated biotinylated-dUTP nick‑end labeling staining suggested that Hax‑1 was involved in RGC apoptosis following ONC. Thus, these results suggested that Hax‑1 may participate in regulating RGC apoptosis via interacting with caspase‑3 and HtrA2 following ONC.