Epithelial-Mesenchymal Transition and its Role in Renal Fibrogenesis

Singh, Brij Mohan Kumar; Mathew, Mary

doi:10.1590/1678-4324-2022210260

Braz. arch. biol. technol.

2022

DOI: 10.1590/1678-4324-2022210260

|View full text |Cite

Epithelial-Mesenchymal Transition and its Role in Renal Fibrogenesis

Brij Mohan Kumar Singh

Mary Mathew

Abstract: Renal fibrosis in chronic renal failure poses a major challenge with regard to providing specific therapeutic strategies. The current hypothesis of the epithelial-mesenchymal transition (EMT) in renal fibrosis proposes that matrix producing fibroblasts and myofibroblasts generated in the diseased kidney causes fibrosis. This paper explores the pathogenetic mechanisms, the role of EMT in renal fibrogenesis in chronic kidney disease, biomarkers, and EMT related anti-fibrotic therapy.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2024

Publication Types

Select...

Article1

Relationship

Self Cite0

Independent1

Authors

Journals

Cited by 1 publication

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Urolithin A Ameliorates the TGF Beta-Dependent Impairment of Podocytes Exposed to High Glucose

Lewko,

Wodzińska,

Daca

et al. 2024

JPM

View full text Add to dashboard Cite

Increased activity of transforming growth factor-beta (TGF-β) is a key factor mediating kidney impairment in diabetes. Glomerular podocytes, the crucial component of the renal filter, are a direct target of TGF-β action, resulting in irreversible cell loss and progression of chronic kidney disease (CKD). Urolithin A (UA) is a member of the family of polyphenol metabolites produced by gut microbiota from ellagitannins and ellagic acid-rich foods. The broad spectrum of biological activities of UA makes it a promising candidate for the treatment of podocyte disorders. In this in vitro study, we investigated whether UA influences the changes exerted in podocytes by TGF-β and high glucose. Following a 7-day incubation in normal (NG, 5.5 mM) or high (HG, 25 mM) glucose, the cells were treated with UA and/or TGF-β1 for 24 h. HG and TGF-β1, each independent and in concert reduced expression of nephrin, increased podocyte motility, and up-regulated expression of b3 integrin and fibronectin. These typical-for-epithelial-to-mesenchymal transition (EMT) effects were inhibited by UA in both HG and NG conditions. UA also reduced the typically elevated HG expression of TGF-β receptors and activation of the TGF-β signal transducer Smad2. Our results indicate that in podocytes cultured in conditions mimicking the diabetic milieu, UA inhibits and reverses changes underlying podocytopenia in diabetic kidneys. Hence, UA should be considered as a potential therapeutic agent in podocytopathies.

show abstract

Urolithin A Ameliorates the TGF Beta-Dependent Impairment of Podocytes Exposed to High Glucose

Lewko,

Wodzińska,

Daca

et al. 2024

JPM

View full text Add to dashboard Cite

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

hi@scite.ai

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Epithelial-Mesenchymal Transition and its Role in Renal Fibrogenesis

Cited by 1 publication

References 60 publications

Urolithin A Ameliorates the TGF Beta-Dependent Impairment of Podocytes Exposed to High Glucose

Urolithin A Ameliorates the TGF Beta-Dependent Impairment of Podocytes Exposed to High Glucose

Contact Info

Product

Resources

About