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The major inflammatory cytokine IL\u20101\u03b2 is associated with intervertebral disc degeneration; however, the molecular mechanisms that drive IL\u20101\u03b2 production in the intervertebral disc, especially in nucleus pulposus (NP) cells, are unknown. In some tissues, advanced glycation end products (AGEs), which accumulate in NP tissues and promote its degeneration, increase oxidative stress and IL\u20101\u03b2 secretion, resulting in disorders, such as obesity, diabetes mellitus and ageing. It remains unclear whether AGEs exhibit similar effects in NP cells. In this study, we observed significant activation of the NLRP3 inflammasome in NP tissues obtained from patients with degenerative disc disease compared to that with idiopathic scoliosis according to results detected by Western blot and immunofluorescence. Using NP cells established from healthy tissues, our <jats:italic>in vitro<\/jats:italic> study revealed that AGEs induced an inflammatory response in NP cells and a degenerative phenotype in a NLRP3\u2010inflammasome\u2010dependent manner related to the receptor for AGEs (RAGE)\/NF\u2010\u03baB pathway and mitochondrial damage induced by mitochondrial reactive oxygen species (mtROS) generation, mitochondrial permeability transition pore (mPTP) activation and calcium mobilization. Among these signals, both RAGE and mitochondrial damage primed NLRP3 and pro\u2010IL\u20101\u03b2 activation as upstream signals of NF\u2010\u03baB activity, whereas mitochondrial damage was critical for the assembly of inflammasome components. These results revealed that accumulation of AGEs in NP tissue may initiate inflammation\u2010related degeneration of the intervertebral disc <jats:italic>via<\/jats:italic> activation of the NLRP3 inflammasome.<\/jats:p>","DOI":"10.1111\/jcmm.13067","type":"journal-article","created":{"date-parts":[[2017,2,22]],"date-time":"2017-02-22T09:12:55Z","timestamp":1487754775000},"page":"1373-1387","source":"Crossref","is-referenced-by-count":125,"title":["Advanced glycation end products regulate anabolic and catabolic activities <i>via<\/i> NLRP3\u2010inflammasome activation in human nucleus pulposus cells"],"prefix":"10.1111","volume":"21","author":[{"given":"Yu","family":"Song","sequence":"first","affiliation":[{"name":"Department of Orthopedics Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Physical Education China University of Geosciences Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yukun","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Orthopedics Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen","family":"Geng","sequence":"additional","affiliation":[{"name":"China Medical University Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Orthopedics First Hospital of Wuhan Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yong","family":"Gao","sequence":"additional","affiliation":[{"name":"Department of Orthopedics Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 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