BMP‑6 protects retinal pigment epithelial cells from oxidative stress‑induced injury by inhibiting the MAPK signaling pathways.

Worldwide, neovascular age‑related macular degeneration (nAMD) is one of the most common causes of blindness in the elderly. In particular, degeneration of retinal pigment epithelial (RPE) cells represents the main pathological process in the development of nAMD, and oxidative stress serves a major role. The present study aimed to investigate the association between bone morphogenetic protein 6 (BMP‑6) and nAMD. BMP‑6 concentration was significantly reduced in patients with wet nAMD compared with in the control group. Furthermore, the present study investigated the protective effects of BMP‑6 on RPE cells following oxidative stress‑induced injury. Cell Counting Kit‑8 assay and terminal deoxynucleotidyl transferase dUTP nick‑end labeling staining demonstrated that BMP‑6 increased RPE cell viability, which was decreased following treatment with hydrogen peroxide (H2O2), and reduced H2O2‑induced apoptosis. In addition, western blotting revealed that BMP‑6 reversed the decrease in pro‑caspase‑3 levels and the dysregulation of the B‑cell lymphoma 2 (Bcl‑2)/Bcl‑2‑associated X protein (Bax) balance caused by H2O2. In addition, alterations in c‑Jun N‑terminal protein kinase (JNK) and p38 mitogen‑activated protein kinase (MAPK) expression were examined, and pretreatment with BMP‑6 was demonstrated to reduce H2O2‑induced activation of JNK and p38 MAPK. Conversely, the effects of BMP‑6 were attenuated by its inhibitor noggin. In conclusion, the present study demonstrated that BMP‑6 may protect RPE cells from oxidative stress injury to a certain extent, which may be associated with alterations in the MAPK signaling pathway. However, the specific mechanism of action underlying this effect requires further investigation. Overall, the present study laid a foundation for exploring novel nAMD treatment methods.