Emerging role and therapeutic implication of mTOR signalling in intervertebral disc degeneration.
Hai-Wei ChenJian-Wei ZhouGuang-Zhi ZhangZhang-Bin LuoLei LiXue-Wen KangPublished in: Cell proliferation (2022)
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.
Keyphrases
- oxidative stress
- induced apoptosis
- endoplasmic reticulum stress
- extracellular matrix
- cell cycle arrest
- cell death
- inflammatory response
- dna damage
- cell proliferation
- signaling pathway
- ischemia reperfusion injury
- protein kinase
- diabetic rats
- spinal cord
- transcription factor
- lipopolysaccharide induced
- stress induced
- spinal cord injury
- immune response
- tyrosine kinase
- replacement therapy
- lps induced