Erratum to: JAK–STAT Signaling as a Target for Inflammatory and Autoimmune Diseases: Current and Future Prospects

Banerjee, Shubhasree; Biehl, Ann; Gadina, Massimo; Hasni, Sarfaraz; Schwartz, Daniella M.

doi:10.1007/s40265-017-0736-y

Cited by 232 publications

(5 citation statements)

References 182 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The JAK-STAT pathway regulates inflammation associated with the pathogenesis of various diseases, including CVDs [12,13,15,22]. In addition, it is emerging as a target in rheumatoid arthritis and chronic myeloproliferative neoplasms, disorders that heighten the CV risk, and atherosclerosis [13].…”

Section: Discussionmentioning

confidence: 99%

High Phosphate-Induced JAK-STAT Signalling Sustains Vascular Smooth Muscle Cell Inflammation and Limits Calcification

Macrì,

Vigorito,

Castiglione

et al. 2023

Biomolecules

View full text Add to dashboard Cite

Vascular calcification (VC) is an age-related complication characterised by calcium-phosphate deposition in the arterial wall driven by the osteogenic transformation of vascular smooth muscle cells (VSMCs). The JAK-STAT pathway is an emerging target in inflammation. Considering the relationship between VC and inflammation, we investigated the role of JAK-STAT signalling during VSMC calcification. Human aortic smooth muscle cells (HASMCs) were cultured in high-inorganic phosphate (Pi) medium for up to 7 days; calcium deposition was determined via Alizarin staining and colorimetric assay. Inflammatory factor secretion was evaluated via ELISA and JAK-STAT members’ activation using Western blot or immunohistochemistry on HASMCs or calcified aortas of Vitamin D-treated C57BL6/J mice, respectively. The JAK-STAT pathway was blocked by JAK Inhibitor I and Von Kossa staining was used for calcium deposits in murine aortic rings. During Pi-induced calcification, HASMCs released IL-6, IL-8, and MCP-1 and activated JAK1-JAK3 proteins and STAT1. Phospho-STAT1 was detected in murine calcified aortas. Blocking of the JAK-STAT cascade reduced HASMC proliferation and pro-inflammatory factor expression and release while increasing calcium deposition and osteogenic transcription factor RUNX2 expression. Consistently, JAK-STAT pathway inhibition exacerbates mouse aortic ring calcification ex vivo. Intriguingly, our results suggest an alternative link between VSMC inflammation and VC.

show abstract

Section: Discussionmentioning

confidence: 99%

High Phosphate-Induced JAK-STAT Signalling Sustains Vascular Smooth Muscle Cell Inflammation and Limits Calcification

Macrì,

Vigorito,

Castiglione

et al. 2023

Biomolecules

View full text Add to dashboard Cite

show abstract

“…Some studies have examined the cytokine patterns of CRS in the Taiwanese populations [39][40][41], but no previous reports have investigated JAK/STAT signaling in CRSwNP for the Taiwanese. Furthermore, many studies focus on development for JAK inhibition (Jakinibs) and novel mechanisms of the JAK/STAT signaling blockade [12,42], and successful use in autoimmune and inflammatory diseases [42].…”

Section: Discussionmentioning

confidence: 99%

JAK2 Phosphorylation Signals and Their Associated Cytokines Involved in Chronic Rhinosinusitis with Nasal Polyps and Correlated with Disease Severity

et al. 2021

View full text Add to dashboard Cite

Janus kinase 2 (JAK2) is a member of the JAK family that transduces cytokine-mediated signals via the JAKs/STATs (signal transducer and activator of transcription proteins) pathway, which plays an important role in many inflammatory diseases. This study investigates the association of p-JAK2 and JAK2-associated cytokines from nasal polyp (NP) tissue with disease severity, and evaluates the p-JAK2-mediated STATs in chronic rhinosinusitis (CRS) with NP. Sixty-one CRSwNP patients with nasal polyps undergoing endoscopic sinus surgery were enrolled, while the turbinate tissues from 26 nasal obstruction patients were examined as the control group. Elevated levels of p-JAK2 were detected in CRSwNP, and significantly correlated with scores of disease severity (LMK-CT, TPS, and SNOT-22). Expressions of the JAK2-associated cytokines, such as IL-5, IL-6, IL-13, G-CSF, and IFN-γ were significantly higher in CRSwNP than in the controls, while the levels of IL-5, IL-6, IL-13, or G-CSF had positive correlation with scores of disease severity. Moreover, markedly increased expression of p-STAT3 in CRSwNP was observed relative to the control. Taken together, these data showed that the JAK2-associated cytokines including IL-6 and G-CSF may stimulate JAK2 phosphorylation to activate p-STAT3, indicating an association with disease severity and supporting its development of JAK2 inhibitor as a potential therapeutic agent for CRS.

show abstract

“…2,3 This binding autophosphorylates the JAK and inputs signals into the nucleus of that immune cell, which activates transcription and regulates gene expression of multiple functions, including immune cell function, hematopoiesis, and antimicrobial and antiviral immunity. [4][5][6] Upadacitinib inhibits the JAK pathway with higher selectivity against JAK1 than the other three subtypes. 2 Specifically, upadacitinib is more than 100-fold more biochemically selective against JAK1 than JAK3 and TYK2, and 60-fold more selective in cellular assays against JAK1 than JAK2.…”

Section: Mechanism Of Actionmentioning

confidence: 99%

“…7 Upadacitinib's specific activity against JAK1 contrasts with tofacitinib, which inhibits JAK1 and JAK3 with some activity against JAK2 and very limited activity against TYK2. [3][4][5] A study assessing the cytokine inhibition of various JAK inhibitors found that upadacitinib was more potent than tofacitinib against IL-2, IL-4, IL-15, IL-21, IL-3, GM-CSF, G-CSF, IFN-gamma stimulated monocytes, and IFN-alpha and had similar potency against IL6, IL10, and IFN-gamma stimulated B cells. 9 When left unchecked, these proinflammatory cytokines can contribute to the inflammatory cascade, leading to mucosal inflammation, damage to the mucosal barrier, and dysregulation of the epithelial layer, and can contribute to further interaction with the immune cells.…”

Section: Mechanism Of Actionmentioning

confidence: 99%

“…9 When left unchecked, these proinflammatory cytokines can contribute to the inflammatory cascade, leading to mucosal inflammation, damage to the mucosal barrier, and dysregulation of the epithelial layer, and can contribute to further interaction with the immune cells. 4 Inhibiting proinflammatory cytokines reduces the overall production of additional cytokines and thereby reduces additional recruitment of immune cells that cause inflammation. This reduction can prevent the chronic cycle of inflammation in immune conditions, including ulcerative colitis.…”

Section: Mechanism Of Actionmentioning

confidence: 99%

See 1 more Smart Citation

Clinical Evaluation of Upadacitinib in the Treatment of Adults with Moderately to Severely Active Ulcerative Colitis (UC): Patient Selection and Reported Outcomes

Irani¹,

Fan²,

Glassner³

et al. 2023

CEG

View full text Add to dashboard Cite

This review addresses appropriate patient selection for upadacitinib, a Janus kinase inhibitor approved by the FDA and EMA for treatment of moderately to severely active ulcerative colitis (UC). Janus kinase molecules can contribute to the inflammatory pathway, so inhibiting certain of them may prove efficacious in treating UC and may reduce safety concerns. Upadacitinib is the newest Janus kinase inhibitor to be approved for UC, so it is timely and relevant to review patient selection and when to consider this medication. We will discuss efficacy and safety data from the pivotal clinical trials on upadacitinib. These data can be shared with patients and can inform the use of these agents in clinical practice.

show abstract

Erratum to: JAK–STAT Signaling as a Target for Inflammatory and Autoimmune Diseases: Current and Future Prospects

Cited by 232 publications

References 182 publications

High Phosphate-Induced JAK-STAT Signalling Sustains Vascular Smooth Muscle Cell Inflammation and Limits Calcification

High Phosphate-Induced JAK-STAT Signalling Sustains Vascular Smooth Muscle Cell Inflammation and Limits Calcification

JAK2 Phosphorylation Signals and Their Associated Cytokines Involved in Chronic Rhinosinusitis with Nasal Polyps and Correlated with Disease Severity

Clinical Evaluation of Upadacitinib in the Treatment of Adults with Moderately to Severely Active Ulcerative Colitis (UC): Patient Selection and Reported Outcomes

Contact Info

Product

Resources

About