Nintedanib ameliorates imiquimod-induced psoriasis in mice by inhibiting NF-κB and VEGFR2 signaling

Li, Xiaohe; Xi, Buri; Yang, Miao; Ma, Xiaoyang; Zhang, Jianwei; Gao, Jingjing; Wei, Wenguo; Yang, Cheng

doi:10.1016/j.intimp.2021.108129

Cited by 10 publications

(2 citation statements)

References 36 publications

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“…This implied that NIN did not directly block receptor activation, at least of PDGF-Rβ and elsewhere, its mechanism of action can include suppression of NFκB signaling 31 . This was pursued through analysis of cytokine-induced activation of the NFκB pathway in CSMC.…”

Section: Resultsmentioning

confidence: 99%

Nintedanib regulates intestinal smooth muscle hyperplasia and phenotype in vitro and in TNBS colitis in vivo

Kataria

Kerr

Lourenssen

et al. 2022

Sci Rep

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Chronic inflammation of the human intestine in Crohn’s disease (CD) causes bowel wall thickening, which typically progresses to stricturing and a recurrent need for surgery. Current therapies have limited success and CD remains idiopathic and incurable. Recent evidence shows a key role of intestinal smooth muscle cell (ISMC) hyperplasia in stricturing, which is not targeted by current anti-inflammatory therapeutics. However, progression of idiopathic pulmonary fibrosis, resembling CD in pathophysiology, is controlled by the tyrosine kinase inhibitors nintedanib (NIN) or pirfenidone, and we investigated these drugs for their effect on ISMC. In a culture model of rat ISMC, NIN inhibited serum- and PDGF-BB-stimulated growth and cell migration, and promoted the differentiated phenotype, while increasing secreted collagen. NIN did not affect signaling through PDGF-Rβ or NFκB but did inhibit cytokine-induced expression of the pro-inflammatory cytokines IL-1β and TNFα, supporting a transcriptional level of control. In TNBS-induced colitis in mice, which resembles CD, NIN decreased ISMC hyperplasia as well as expression of TNFα and IL-1β, without effect in control animals. NIN also inhibited growth of human ISMC in response to human serum or PDGF-BB, which further establishes a broad range of actions of NIN that support further trial in human IBD.

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Section: Resultsmentioning

confidence: 99%

Nintedanib regulates intestinal smooth muscle hyperplasia and phenotype in vitro and in TNBS colitis in vivo

Kataria

Kerr

Lourenssen

et al. 2022

Sci Rep

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“…Cell viability was measured using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) and CCK‐8 as previously described. 14 …”

Section: Methodsmentioning

confidence: 99%

Duvelisib attenuates bleomycin‐induced pulmonary fibrosis via inhibiting the PI3K/Akt/mTOR signalling pathway

Yang

et al. 2023

J Cellular Molecular Medi

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New fluorinated diarylureas linked to pyrrolo[2,3-d]pyrimidine scaffold as VEGFR-2 inhibitors: Molecular docking and biological evaluation

Adel

Abouzid

2022

Bioorganic Chemistry

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Nintedanib ameliorates imiquimod-induced psoriasis in mice by inhibiting NF-κB and VEGFR2 signaling

Cited by 10 publications

References 36 publications

Nintedanib regulates intestinal smooth muscle hyperplasia and phenotype in vitro and in TNBS colitis in vivo

Nintedanib regulates intestinal smooth muscle hyperplasia and phenotype in vitro and in TNBS colitis in vivo

Duvelisib attenuates bleomycin‐induced pulmonary fibrosis via inhibiting the PI3K/Akt/mTOR signalling pathway

New fluorinated diarylureas linked to pyrrolo[2,3-d]pyrimidine scaffold as VEGFR-2 inhibitors: Molecular docking and biological evaluation

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