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Diverse Role of TGF-β in Kidney Disease

Yue-Yu Gu1,2, Xu-Sheng Liu1, Xiao-Ru Huang2,3

  • 1Guangdong Provincial Key Laboratory of Clinical Research on Traditional Chinese Medicine Syndrome, Department of Nephrology, Guangdong Provincial Hospital of Chinese Medicine, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, China.

Frontiers in Cell and Developmental Biology
|April 8, 2020
PubMed

Insights

Transforming growth factor-β (TGF-β) paradoxically impacts kidney disease by mediating fibrosis and inflammation. Targeting its downstream Smad signaling offers novel therapeutic strategies for chronic kidney disease (CKD).

Area of Science:

  • Nephrology
  • Molecular Biology
  • Immunology

Background:

  • Chronic kidney disease (CKD) is characterized by inflammation and fibrosis.
  • Transforming growth factor-β (TGF-β) plays a dual role in CKD, mediating fibrosis and suppressing inflammation.
  • TGF-β blockade inhibits fibrosis but exacerbates inflammation, highlighting its complex role.

Purpose of the Study:

  • To discuss the paradoxical functions of TGF-β1 in regulating renal inflammation and fibrosis.
  • To elucidate the underlying molecular mechanisms involving TGF-β/Smad signaling.
  • To highlight novel therapeutic strategies targeting downstream signaling pathways for kidney disease.

Main Methods:

  • Review of existing literature on TGF-β1, Smad signaling, and non-coding RNAs in CKD.
  • Analysis of the transcriptional regulation of renal inflammation and fibrosis by Smad3 and Smad7.
  • Discussion of therapeutic approaches focusing on rebalancing Smad3/Smad7 signaling.

Main Results:

  • TGF-β1 activates Smad3 and Smad3-dependent non-coding RNAs, differentially regulating renal inflammation and fibrosis.
  • Smad7 negatively regulates the TGF-β1 signaling pathway.
  • Targeting Smad3-dependent non-coding RNAs presents a potential therapeutic avenue.

Conclusions:

  • Understanding the dual role of TGF-β1 is crucial for developing effective CKD treatments.
  • Rebalancing Smad3/Smad7 signaling offers a promising therapeutic strategy.
  • Targeting downstream TGF-β/Smad signaling and transcriptomes could lead to novel treatments for kidney disease.
Keywords:
SmadsTGF-βfibrosisinflammationmechanismstherapy

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