STAT1 as a novel therapeutical target in pro-atherogenic signal integration of IFNγ, TLR4 and IL-6 in vascular disease

HDAC inhibitor–dependent transcriptome and memory reinstatement in cognitive decline models

“…Thus, antiinflammatory effects of SAHA are likely to be mediated via processes that involve nonhistone protein acetylation, which is supported by recent findings (90,91). Consistent with these data, we found that at least part of the inflammatory response might be mediated by the action of transcription factors such as STAT1, which are regulated by acetylation (41,92,93) and have been shown to control inflammatory processes (94,95). Our data suggest that SAHA treatment indirectly ameliorates the age-associated increase in STAT1 activity.…”

Axl modulates immune activation of smooth muscle cells in vein graft remodeling

“…Two regulatory mechanisms have been described in controlling MHC II transactivator (CIITA) activity, involving peroxisome proliferator-activated receptor-␥ and histone deacetylase 2 (12, 13). The major downstream target for IFN-␥ in vascular diseases is STAT1 (21,29). To date, only one study (35) in mesangial cells has suggested a connection between Axl and STAT1 signaling.…”

“…6A). The inhibitory protein SOCS1 is the primary regulator of STAT1 signaling in SMCs (29). SOCS1 is also an important mediator of the TAM family in inhibition of STAT1/STAT3-dependent cytokine production in innate immune cells (27).…”

Gene delivery of suppressors of cytokine signaling (SOCS) inhibits inflammation and atherosclerosis development in mice

“…Different JAK/STAT components have been detected in the heart and also in the inflammatory regions of human atherosclerotic plaques [3,7,16,22,24,31]. In experimental models, either gene deficiency or pharmacological inhibition of JAK2, STAT1 and STAT3 prevented atherosclerotic lesion formation [1,5,7,16,28].…”