S Chen1, S Liu1, K Ma1, L Zhao1, H Lin1, Z Shao2. 1. Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. 2. Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Electronic address: szwpro@163.com.
Abstract
OBJECTIVE: This paper aims to provide a comprehensive review of the changing role of transforming growth factor-β (TGF-β) signaling in intervertebral disc (IVD) health and disease. METHODS: A comprehensive literature search was performed using PubMed terms 'TGF-β' and 'IVD'. RESULTS: TGF-β signaling is necessary for the development and growth of IVD, and can play a protective role in the restoration of IVD tissues by stimulating matrix synthesis, inhibiting matrix catabolism, inflammatory response and cell loss. However, excessive activation of TGF-β signaling is detrimental to the IVD, and inhibition of the aberrant TGF-β signaling can delay IVD degeneration. CONCLUSIONS: Activation of TGF-β signaling has a promising treatment prospect for IVD degeneration, while excessive activation of TGF-β signaling may contribute to the progression of IVD degeneration. Studies aimed at elucidating the changing role of TGF-β signaling in IVD at different pathophysiological stages and its specific molecular mechanisms are needed, and these studies will contribute to safe and effective TGF-β signaling-based treatments for IVD degeneration.
OBJECTIVE: This paper aims to provide a comprehensive review of the changing role of transforming growth factor-β (TGF-β) signaling in intervertebral disc (IVD) health and disease. METHODS: A comprehensive literature search was performed using PubMed terms 'TGF-β' and 'IVD'. RESULTS: TGF-β signaling is necessary for the development and growth of IVD, and can play a protective role in the restoration of IVD tissues by stimulating matrix synthesis, inhibiting matrix catabolism, inflammatory response and cell loss. However, excessive activation of TGF-β signaling is detrimental to the IVD, and inhibition of the aberrant TGF-β signaling can delay IVD degeneration. CONCLUSIONS: Activation of TGF-β signaling has a promising treatment prospect for IVD degeneration, while excessive activation of TGF-β signaling may contribute to the progression of IVD degeneration. Studies aimed at elucidating the changing role of TGF-β signaling in IVD at different pathophysiological stages and its specific molecular mechanisms are needed, and these studies will contribute to safe and effective TGF-β signaling-based treatments for IVD degeneration.