Reciprocal regulation of TGF-β and reactive oxygen species: A perverse cycle for fibrosis
By Rui‐Ming Liu, L. Desai. Redox Biology, 2015
636 citations recorded by the source corpus.
Transforming growth factor beta (TGF-β) is the most potent pro-fibrogenic cytokine and its expression is increased in almost all of fibrotic diseases. Although signaling through Smad pathway is believed to play a central role in TGF-β's fibrogenesis, emerging evidence indicates that reactive oxygen species (ROS) modulate TGF-β's signaling through different pathways including Smad pathway. TGF-β1 increases ROS production and suppresses antioxidant enzymes, leading to a redox imbalance. ROS, in turn, induce/activate TGF-β1 and mediate many of TGF-β's fibrogenic effects, forming a vicious cycle (see graphic flow chart on the right). Here, we review the current knowledge on the feed-forward mechanisms between TGF-β1 and ROS in the development of fibrosis. Therapeutics targeting TGF-β-induced and ROS-dependent cellular signaling represents a novel approach in the treatment of fibrotic disorders.
Subfields: Molecular Biology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/c894e87083203f9e3ecf0aa6cc739af053d80ae2
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Citations in the corpus
- Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives (2020, background): “Finally, it was shown that ROS can act as inducer or effector of the TGF-β signaling and therefore generate a vicious cycle for fibrosis [145].”
- New insights into TGF-β/Smad signaling in tissue fibrosis. (2018, background): “TGF-β1 was the most fibrogenic cytokine in liver which was derived from paracrine and autocrine sources [48].”
- TGF-β in Hepatic Stellate Cell Activation and Liver Fibrogenesis—Updated 2019 (2019, background): “On the other hand, TGF-β augments mitochondrial ROS production by activating the mTOR pathway and reducing the activity of complex III and IV [147].”