Nintedanib downregulates the transition of cultured systemic sclerosis fibrocytes into myofibroblasts and their pro-fibrotic activity

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 1478-6362

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Nintedanib downregulates the transition of cultured systemic sclerosis fibrocytes into myofibroblasts and their pro-fibrotic activity ; volume:23 ; number:1 ; day:3 ; month:8 ; year:2021 ; pages:1-11 ; date:12.2021
Arthritis Research & Therapy ; 23, Heft 1 (3.8.2021), 1-11, 12.2021

Creator: Cutolo, Maurizio
Gotelli, Emanuele
Montagna, Paola
Tardito, Samuele
Paolino, Sabrina
Pizzorni, Carmen
Sulli, Alberto
Smith, Vanessa
Soldano, Stefano

Contributor: SpringerLink (Online service)

DOI: 10.1186/s13075-021-02555-2

URN: urn:nbn:de:101:1-2021102923523569021037

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 15.08.2025, 7:34 AM CEST

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Associated

Cutolo, Maurizio
Gotelli, Emanuele
Montagna, Paola
Tardito, Samuele
Paolino, Sabrina
Pizzorni, Carmen
Sulli, Alberto
Smith, Vanessa
Soldano, Stefano
SpringerLink (Online service)

Other Objects (12)

Correction: Nintedanib downregulates the transition of cultured systemic sclerosis fibrocytes into myofibroblasts and their pro-fibrotic activity

Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease

Correction: Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease

Extracellular vesicles from steatotic hepatocytes provoke pro-fibrotic responses in cultured stellate cells

Nintedanib: A Review in Fibrotic Interstitial Lung Diseases

Correction to: Nintedanib: A Review in Fibrotic Interstitial Lung Diseases

O-GlcNAcylation controls pro-fibrotic transcriptional regulatory signaling in myofibroblasts

Early activation of pro-fibrotic WNT5A in sepsis-induced acute lung injury

Regulation of fibroblast Fas expression by soluble and mechanical pro-fibrotic stimuli

Dipeptidyl peptidase-4-mediated fibronectin processing evokes a pro-fibrotic extracellular matrix

Pro-fibrotic effects of CCL18 on human lung fibroblasts are mediated via CCR6

Correction: Nintedanib downregulates the transition of cultured systemic sclerosis fibrocytes into myofibroblasts and their pro-fibrotic activity

Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease

Correction: Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease

Extracellular vesicles from steatotic hepatocytes provoke pro-fibrotic responses in cultured stellate cells

Nintedanib: A Review in Fibrotic Interstitial Lung Diseases

Correction to: Nintedanib: A Review in Fibrotic Interstitial Lung Diseases

O-GlcNAcylation controls pro-fibrotic transcriptional regulatory signaling in myofibroblasts

Early activation of pro-fibrotic WNT5A in sepsis-induced acute lung injury

Regulation of fibroblast Fas expression by soluble and mechanical pro-fibrotic stimuli

Dipeptidyl peptidase-4-mediated fibronectin processing evokes a pro-fibrotic extracellular matrix

Pro-fibrotic effects of CCL18 on human lung fibroblasts are mediated via CCR6

Correction: Nintedanib downregulates the transition of cultured systemic sclerosis fibrocytes into myofibroblasts and their pro-fibrotic activity

Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease

Correction: Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease

Extracellular vesicles from steatotic hepatocytes provoke pro-fibrotic responses in cultured stellate cells

Nintedanib: A Review in Fibrotic Interstitial Lung Diseases

Correction to: Nintedanib: A Review in Fibrotic Interstitial Lung Diseases

O-GlcNAcylation controls pro-fibrotic transcriptional regulatory signaling in myofibroblasts

Early activation of pro-fibrotic WNT5A in sepsis-induced acute lung injury

Regulation of fibroblast Fas expression by soluble and mechanical pro-fibrotic stimuli

Dipeptidyl peptidase-4-mediated fibronectin processing evokes a pro-fibrotic extracellular matrix

Pro-fibrotic effects of CCL18 on human lung fibroblasts are mediated via CCR6

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Nintedanib downregulates the transition of cultured systemic sclerosis fibrocytes into myofibroblasts and their pro-fibrotic activity

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Other Objects (12)

Correction: Nintedanib downregulates the transition of cultured systemic sclerosis fibrocytes into myofibroblasts and their pro-fibrotic activity

Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease

Correction: Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease

Extracellular vesicles from steatotic hepatocytes provoke pro-fibrotic responses in cultured stellate cells

Nintedanib: A Review in Fibrotic Interstitial Lung Diseases

Correction to: Nintedanib: A Review in Fibrotic Interstitial Lung Diseases

O-GlcNAcylation controls pro-fibrotic transcriptional regulatory signaling in myofibroblasts

Early activation of pro-fibrotic WNT5A in sepsis-induced acute lung injury

Regulation of fibroblast Fas expression by soluble and mechanical pro-fibrotic stimuli

Dipeptidyl peptidase-4-mediated fibronectin processing evokes a pro-fibrotic extracellular matrix

Pro-fibrotic effects of CCL18 on human lung fibroblasts are mediated via CCR6

Pro-fibrotic effects of CCL18 on human lung fibroblasts are mediated via CCR6

Correction: Nintedanib downregulates the transition of cultured systemic sclerosis fibrocytes into myofibroblasts and their pro-fibrotic activity

Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease

Correction: Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease

Extracellular vesicles from steatotic hepatocytes provoke pro-fibrotic responses in cultured stellate cells

Nintedanib: A Review in Fibrotic Interstitial Lung Diseases

Correction to: Nintedanib: A Review in Fibrotic Interstitial Lung Diseases

O-GlcNAcylation controls pro-fibrotic transcriptional regulatory signaling in myofibroblasts

Early activation of pro-fibrotic WNT5A in sepsis-induced acute lung injury

Regulation of fibroblast Fas expression by soluble and mechanical pro-fibrotic stimuli

Dipeptidyl peptidase-4-mediated fibronectin processing evokes a pro-fibrotic extracellular matrix

Pro-fibrotic effects of CCL18 on human lung fibroblasts are mediated via CCR6

Pro-fibrotic effects of CCL18 on human lung fibroblasts are mediated via CCR6

Correction: Nintedanib downregulates the transition of cultured systemic sclerosis fibrocytes into myofibroblasts and their pro-fibrotic activity

Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease

Correction: Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease

Extracellular vesicles from steatotic hepatocytes provoke pro-fibrotic responses in cultured stellate cells

Nintedanib: A Review in Fibrotic Interstitial Lung Diseases

Correction to: Nintedanib: A Review in Fibrotic Interstitial Lung Diseases

O-GlcNAcylation controls pro-fibrotic transcriptional regulatory signaling in myofibroblasts

Early activation of pro-fibrotic WNT5A in sepsis-induced acute lung injury

Regulation of fibroblast Fas expression by soluble and mechanical pro-fibrotic stimuli

Dipeptidyl peptidase-4-mediated fibronectin processing evokes a pro-fibrotic extracellular matrix

Pro-fibrotic effects of CCL18 on human lung fibroblasts are mediated via CCR6

Pro-fibrotic effects of CCL18 on human lung fibroblasts are mediated via CCR6

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