Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8310080 | Clinica Chimica Acta | 2016 | 34 Pages |
Abstract
Autophagy is a homeostatic mechanism through which intracellular damaged organelles and proteins are degraded and recycled in response to increased metabolic demands or stresses. Although primarily cytoprotective, dysfunction of autophagy is often associated with many degenerative diseases, including intervertebral disc (IVD) degeneration (IDD). As a main contributing factor to low back pain, IDD is the pathological basis for various debilitating spinal diseases. Either higher or lower levels of autophagy are observed in degenerative IVD cells. Despite the precise role of autophagy in disc degeneration that is still controversial, with difference from protection to aggravation, targeting autophagy has shown promise for mitigating disc degeneration. In the current review, we summarize the changes of autophagy in degenerative IVD cells and mainly discuss the relationship between autophagy and IDD. With continued efforts, modulation of the autophagic process could be a potential and attractive therapeutic strategy for degenerative disc disease.
Keywords
ECMIVDIDDADAMTSCol IImTORC1LAMP2AGRP783-MALC3ATGCEPSIL-1βLBPHsc70miRNAsSirt1NF-κBMMPDfcp1TGF-β1double FYVE-containing protein 1Jnk3-methyladeninec-Jun N-terminal kinaseERK1/2ULKHydrogen peroxideAutophagyInterleukin-1βTransforming growth factor-β1tumor necrosis factor-αIntervertebral disk degenerationIntervertebral diskmicroRNAsTNF-αnuclear factor-κBphosphatidyl ethanolamineAnnulus fibrosusLAMP-2Extracellular matrixMatrix metalloproteinasesMammalian target of rapamycin complex 1Nucleus pulposusH2O2microtubule-associated protein 1 light chain 3autophagy-related genesCol Iclass III phosphatidylinositol 3-kinaseType I collagenType II collagenLow back painextracellular signal-regulated kinase 1/2glucose regulated protein 78
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Authors
Shu-Jun Zhang, Wei Yang, Cheng Wang, Wen-Si He, Hai-Yang Deng, Yi-Guo Yan, Jian Zhang, Yong-Xiao Xiang, Wen-Jun Wang,