2015
DOI: 10.1016/j.intimp.2015.05.036
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10-Hydroxy-2-decenoic acid inhibiting the proliferation of fibroblast-like synoviocytes by PI3K–AKT pathway

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Cited by 16 publications
(16 citation statements)
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“…Histone deacetylase inhibition by 10-HDA is thought to reactivate the expression of epigenetically silenced genes in mammalian cells, leading to the hypothesis that a similar effect could be at the basis of caste switching in bees (Spannhoff et al, 2011). Modifications of histone acetylation have also emerged from a study showing 10-HDA inhibition of fibroblast-like synoviocytes from rheumatoid arthritis patients, suggesting potential therapeutic effects against chronic inflammation degenerative disease (Wang et al, 2015). …”
Section: Royal Jellymentioning
confidence: 99%
“…Histone deacetylase inhibition by 10-HDA is thought to reactivate the expression of epigenetically silenced genes in mammalian cells, leading to the hypothesis that a similar effect could be at the basis of caste switching in bees (Spannhoff et al, 2011). Modifications of histone acetylation have also emerged from a study showing 10-HDA inhibition of fibroblast-like synoviocytes from rheumatoid arthritis patients, suggesting potential therapeutic effects against chronic inflammation degenerative disease (Wang et al, 2015). …”
Section: Royal Jellymentioning
confidence: 99%
“…Phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signalling pathway was reported in SFs; there, it showed an unusual activation state, which might lead to the imbalance of SFs proliferation and apoptosis. It was also shown that the gene coding for the PIK3R2 was targeted by microRNA-126 [ 34 , 35 ]. Gao et al aimed to explore the associations between miR-126, PIK3R2 gene and PI3K/AKT signalling pathway in RASFs [ 36 ].…”
Section: Autoimmune Diseases Related To Mir-126mentioning
confidence: 99%
“…Other general inhibitors, some of which are in clinical trials for various cancers, decrease RA FLS proliferation or disease severity in mouse models of RA and include phenylbutyrate [58], romidepsin (FK228) (Figure 3) [61], entinostat (MS-275) [62], zolinza (suberoylanilide hydroxamic acid) [63] and 10-hydroxy-2-decanoic acid [64]. Although promising, HDACs have different patterns of expression and function in RA FLS as previously discussed, and so a specific HDAC inhibitor profile could be important.…”
Section: Hdac Inhibition In Ra Fls and In Arthritismentioning
confidence: 99%