Emerging role and therapeutic implication of mTOR signalling in intervertebral disc degeneration

Intervertebral disc degeneration (IDD), an important cause of chronic low back pain (LBP), is considered the pathological basis for various spinal degenerative diseases. A series of factors, including inflammatory response, oxidative stress, autophagy, abnormal mechanical stress, nutritional deficiency, and genetics, lead to reduced extracellular matrix (ECM) synthesis by intervertebral disc (IVD) cells and accelerate IDD progression. Mammalian target of rapamycin (mTOR) is an evolutionarily conserved serine/threonine kinase that plays a vital role in diverse degenerative diseases. Recent studies have shown that mTOR signalling is involved in the regulation of autophagy, oxidative stress, inflammatory responses, ECM homeostasis, cellular senescence, and apoptosis in IVD cells. Accordingly, we reviewed the mechanism of mTOR signalling in the pathogenesis of IDD to provide innovative ideas for future research and IDD treatment.

Automated summary

Intervertebral disc degeneration (IDD) is an important cause of chronic low back pain (LBP) and serves as the pathological basis for various spinal degenerative diseases. Factors such as autophagy, oxidative stress, inflammatory responses, ECM homeostasis, cellular senescence, and apoptosis are involved in reducing ECM synthesis by intervertebral disc (IVD) cells and accelerating IDD progression. The mTOR signaling pathway plays a crucial role in the regulation of autophagy, oxidative stress, inflammatory responses, ECM homeostasis, cellular senescence, and apoptosis in IVD cells.