Near Infrared Responsive Gold Nanorods Attenuate Osteoarthritis Progression by Targeting TRPV1

Near Infrared Responsive Gold Nanorods Attenuate Osteoarthritis Progression by Targeting TRPV1

2024 | Weitong Li, Zhongyang Lv, Peng Wang, Ya Xie, Wei Sun, Hu Guo, Xiaoyu Jin, Yuan Liu, Ruiyang Jiang, Yuxiang Fei, Guihua Tan, Huiming Jiang, Xucai Wang, Zizheng Liu, Zheng Wang, Nuo Xu, Wenli Gong, Rui Wu, and Dongquan Shi
This study investigates the potential of near-infrared (NIR)-responsive gold nanorods (AuNRs) conjugated with a TRPV1 monoclonal antibody (Cit-AuNRs@Anti-TRPV1) to treat osteoarthritis (OA). TRPV1 activation has been shown to alleviate cartilage degeneration by suppressing chondrocyte ferroptosis. The researchers synthesized Cit-AuNRs and conjugated them with Anti-TRPV1, creating a photothermal switch that can be activated by NIR irradiation. This system effectively activated TRPV1 and reduced cartilage degradation in a mouse model of OA. The treatment also improved physical activities and reduced pain in mice with destabilization of the medial meniscus (DMM)-induced OA. Additionally, it suppressed macrophagic inflammation and bone remodeling, further enhancing the therapeutic effects. The study provides a promising strategy for the targeted treatment of OA by protecting chondrocytes from ferroptosis.This study investigates the potential of near-infrared (NIR)-responsive gold nanorods (AuNRs) conjugated with a TRPV1 monoclonal antibody (Cit-AuNRs@Anti-TRPV1) to treat osteoarthritis (OA). TRPV1 activation has been shown to alleviate cartilage degeneration by suppressing chondrocyte ferroptosis. The researchers synthesized Cit-AuNRs and conjugated them with Anti-TRPV1, creating a photothermal switch that can be activated by NIR irradiation. This system effectively activated TRPV1 and reduced cartilage degradation in a mouse model of OA. The treatment also improved physical activities and reduced pain in mice with destabilization of the medial meniscus (DMM)-induced OA. Additionally, it suppressed macrophagic inflammation and bone remodeling, further enhancing the therapeutic effects. The study provides a promising strategy for the targeted treatment of OA by protecting chondrocytes from ferroptosis.
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