Current osteoporosis reports · 2019
Pro-inflammatory Cytokines and Osteocytes.
СтатьяПоддержка исследования: вне правительства СШАОбзорНазвание и аннотация: Перевод в очереди
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Zhou Miao, Li Shuyi, Pathak Janak L
Аннотация
PURPOSE OF REVIEW: An elevated level of pro-inflammatory cytokines in inflammatory conditions causes bone loss and disrupts vital organ function. Osteocytes comprise > 95% of the cellular component in bone tissue, produce a range of cytokines and signaling molecules, and influence bone and other organ function. In this review, we hypothesized that an elevated level of pro-inflammatory cytokines in inflammatory conditions affects osteocyte survival and function thereby possibly amplifying inflammation, and causing bone loss and non-bone clinical complications.
RECENT FINDINGS: Several studies have reported that the elevated level of pro-inflammatory cytokines in inflammatory conditions alters osteocyte mechanosensitivity, causes osteocyte apoptosis, and modulates osteocyte-derived production of various inflammatory cytokines and signaling molecules. Cytokines and signaling molecules released from osteocytes affect surrounding bone cells and distant organ function in a paracrine and endocrine fashion. Inflammatory diseases including diabetes, chronic kidney disease, rheumatoid arthritis, and periodontitis affect osteocyte survival and function, and upregulate osteocyte-derived expression of sclerostin, RANKL, TNFα, FGF23, DKK1, and other signaling molecules.
RECENT FINDINGS: Several studies have reported that the elevated level of pro-inflammatory cytokines in inflammatory conditions alters osteocyte mechanosensitivity, causes osteocyte apoptosis, and modulates osteocyte-derived production of various inflammatory cytokines and signaling molecules. Cytokines and signaling molecules released from osteocytes affect surrounding bone cells and distant organ function in a paracrine and endocrine fashion. Inflammatory diseases including diabetes, chronic kidney disease, rheumatoid arthritis, and periodontitis affect osteocyte survival and function, and upregulate osteocyte-derived expression of sclerostin, RANKL, TNFα, FGF23, DKK1, and other signaling molecules.