ArticleMediators of inflammation2015
TGF-Beta Blockade Increases Renal Inflammation Caused by the C-Terminal Module of the CCN2.
Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Serial Combination of Toxic and Ischemic Renal Damages Causes Subsequent Chronic, Irreversible, and Progressive Renal Disease in Rats.International journal of molecular sciences · 2025Article
- Oxy210, a Semi-Synthetic Oxysterol, Exerts Anti-Inflammatory Effects in Macrophages via Inhibition of Toll-like Receptor (TLR) 4 and TLR2 Signaling and Modulation of Macrophage Polarization.International journal of molecular sciences · 2022Article
- Targeting the progression of chronic kidney disease.Nature reviews. Nephrology · 2020Review
- Gene expression profiling analysis reveals that the long non‑coding RNA uc.412 is involved in mesangial cell proliferation.Molecular medicine reports · 2019Article
- Conditional knockout of TGF-βRII /Smad2 signals protects against acute renal injury by alleviating cell necroptosis, apoptosis and inflammation.Theranostics · 2019Article
- LncRNAs in TGF-β-Driven Tissue Fibrosis.Non-coding RNA · 2018Review
- Transforming growth factor-β signalling in renal fibrosis: from Smads to non-coding RNAs.The Journal of physiology · 2018Review
- Redirecting TGF-Journal of the American Society of Nephrology : JASN · 2018Article
- Bioscreening and expression of a camel anti-CTGF VHH nanobody and its renaturation by a novel dialysis-dilution method.AMB Express · 2016Article
- Dysregulation of TGFβ1 Activity in Cancer and Its Influence on the Quality of Anti-Tumor Immunity.Journal of clinical medicine · 2016Review
- Citrate Attenuates Adenine-Induced Chronic Renal Failure in Rats by Modulating the Th17/Treg Cell Balance.Inflammation · 2016Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CCN family member 2 (CCN2, also known as connective tissue growth factor) may behave as a risk biomarker and a potential therapeutic target for renal disease. CCN2 participates in the regulation of inflammation and fibrosis. TGF-β is considered the main fibrogenic cytokine; however, in some pathological settings TGF-β also has anti-inflammatory properties. CCN2 has been proposed as a downstream profibrotic mediator of TGF-β, but data on TGF-β role in CCN2 actions are scarce. Our aim was to evaluate the effect of TGF-β blockade in CCN2-mediated experimental renal damage. Systemic administration of the C-terminal module of CCN2 to mice caused sustained renal inflammation. In these mice, TGF-β blockade, using an anti-TGF-β neutralizing antibody, significantly increased renal expression of the NGAL (a kidney injury biomarker), kidney infiltration by monocytes/macrophages, and upregulation of MCP-1 expression. The anti-inflammatory effect of TGF-β seems to be mediated by a dysregulation of the systemic Treg immune response, shown by decreased levels of circulating CD4(+)/Foxp3(+)Treg cells. Our experimental data support the idea that TGF-β exerts anti-inflammatory actions in the kidney and suggest that it is not an optimal therapeutic target.
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