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Mediterr J Rheumatol 2022;33(2):176-84
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TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases
Aglaia Chalkia1, Harikleia Gakiopoulou2, Irini Theochari2, Periklis G. Foukas3, Dimitrios Vassilopoulos4, Dimitrios Petras1
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1Nephrology Department, Hippokration General Hospital, Athens, Greece

21st Department of Pathology, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece

32nd Department of Pathology, National and Kapodistrian University of Athens, School of Medicine, Athens, Attikon University Hospital, Athens, Greece

42nd Department of Medicine and Laboratory, Clinical Immunology - Rheumatology Unit, National and Kapodistrian University of Athens, School of Medicine, Athens, Greece

Abstract

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.

Cite this article as: Chalkia A, Gakiopoulou H, Theochari I, Foukas PG, Vassilopoulos D, Petras D. TGF-β1/Smad Signalling in Proliferative Glomerulonephritis Associated with Autoimmune Diseases. Mediterr J Rheumatol 2022;33(2):176-84

Article Submitted: 31 May 2021; Revised Form: 4 Sep 2021; Article Accepted: 15 Sep 2021; Available Online: 30 Jun 2022

https://doi.org/10.31138/mjr.33.2.176

This work is licensed under a Creative Commons Attribution 4.0 International License (CC-BY).

©Chalkia A, Gakiopoulou H, Theochari I, Foukas PG, Vassilopoulos D, Petras D.

Keywords: proliferative glomerulonephritis, TGF-β1/Smad signalling, fibrosis, inflammation