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TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases

Glomerulonephritis is a common cause of chronic kidney disease, which has emerged as a major cause of end-stage renal disease. Autoimmune diseases, such as Systemic Lupus Erythematosus (SLE) and ANCA-associated vasculitis (AAV) are often associated with proliferative glomerulonephritis. Transforming...

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Autores principales: Chalkia, Aglaia, Gakiopoulou, Harikleia, Theochari, Irini, Foukas, Periklis G., Vassilopoulos, Dimitrios, Petras, Dimitrios
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Mediterranean Journal of Rheumatology (MJR) 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9450207/
https://www.ncbi.nlm.nih.gov/pubmed/36128207
http://dx.doi.org/10.31138/mjr.33.2.176
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author Chalkia, Aglaia
Gakiopoulou, Harikleia
Theochari, Irini
Foukas, Periklis G.
Vassilopoulos, Dimitrios
Petras, Dimitrios
author_facet Chalkia, Aglaia
Gakiopoulou, Harikleia
Theochari, Irini
Foukas, Periklis G.
Vassilopoulos, Dimitrios
Petras, Dimitrios
author_sort Chalkia, Aglaia
collection PubMed
description Glomerulonephritis is a common cause of chronic kidney disease, which has emerged as a major cause of end-stage renal disease. Autoimmune diseases, such as Systemic Lupus Erythematosus (SLE) and ANCA-associated vasculitis (AAV) are often associated with proliferative glomerulonephritis. Transforming growth factor-β1 (TGF-β1) is a cytokine with pleiotropic effects in chronic renal diseases, based on in vivo and in vitro studies. The Smad-dependent signalling pathway plays an important role in the regulation of renal fibrosis (excessive production of extracellular matrix [ECM]) and inflammation. However, clinical trials targeting TGF-β1 have presented disappointing results, suggesting that the downstream signalling is quite complex. The diversity of the effects may associate with the interactions between TGF-β1 signalling and other downstream signalling, as well as the different cellular responses, which TGF-β1 promotes. Recently, macrophage chemoattract and epigenetic effects have also been identified as new mechanisms, wherefore TGF-β1/Smad signalling mediates renal injury. This review provides an overview of the role of TGF-β1/Smad signalling pathway from in vivo and in vitro studies in the pathogenesis of glomerulonephritis and particularly in proliferative glomerulonephritis, which is associated with autoimmune diseases.
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spelling pubmed-94502072022-09-19 TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases Chalkia, Aglaia Gakiopoulou, Harikleia Theochari, Irini Foukas, Periklis G. Vassilopoulos, Dimitrios Petras, Dimitrios Mediterr J Rheumatol Review Glomerulonephritis is a common cause of chronic kidney disease, which has emerged as a major cause of end-stage renal disease. Autoimmune diseases, such as Systemic Lupus Erythematosus (SLE) and ANCA-associated vasculitis (AAV) are often associated with proliferative glomerulonephritis. Transforming growth factor-β1 (TGF-β1) is a cytokine with pleiotropic effects in chronic renal diseases, based on in vivo and in vitro studies. The Smad-dependent signalling pathway plays an important role in the regulation of renal fibrosis (excessive production of extracellular matrix [ECM]) and inflammation. However, clinical trials targeting TGF-β1 have presented disappointing results, suggesting that the downstream signalling is quite complex. The diversity of the effects may associate with the interactions between TGF-β1 signalling and other downstream signalling, as well as the different cellular responses, which TGF-β1 promotes. Recently, macrophage chemoattract and epigenetic effects have also been identified as new mechanisms, wherefore TGF-β1/Smad signalling mediates renal injury. This review provides an overview of the role of TGF-β1/Smad signalling pathway from in vivo and in vitro studies in the pathogenesis of glomerulonephritis and particularly in proliferative glomerulonephritis, which is associated with autoimmune diseases. The Mediterranean Journal of Rheumatology (MJR) 2022-06-30 /pmc/articles/PMC9450207/ /pubmed/36128207 http://dx.doi.org/10.31138/mjr.33.2.176 Text en © 2022 The Mediterranean Journal of Rheumatology (MJR) https://creativecommons.org/licenses/by/4.0/This work is licensed under and Creative Commons Attribution-NonCommercial 4.0 International License.
spellingShingle Review
Chalkia, Aglaia
Gakiopoulou, Harikleia
Theochari, Irini
Foukas, Periklis G.
Vassilopoulos, Dimitrios
Petras, Dimitrios
TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases
title TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases
title_full TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases
title_fullStr TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases
title_full_unstemmed TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases
title_short TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases
title_sort tgf-β1/smad signalling in proliferative glomerulonephritis associated with autoimmune diseases
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9450207/
https://www.ncbi.nlm.nih.gov/pubmed/36128207
http://dx.doi.org/10.31138/mjr.33.2.176
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