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TGF-β1/Smads and miR-21 in Renal Fibrosis and Inflammation
Agnieszka Loboda1, Mateusz Sobczak1, Alicja Jozkowicz1
1Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, 30-387 Kraków, Poland.
Abstract:
Renal fibrosis, irrespective of its etiology, is a final common stage of almost all chronic kidney diseases. Increased apoptosis, epithelial-to-mesenchymal transition, and inflammatory cell infiltration characterize the injured kidney. On the molecular level, transforming growth factor-β1 (TGF-β1)-Smad3 signaling pathway plays a central role in fibrotic kidney disease. Recent findings indicate the prominent role of microRNAs, small noncoding RNA molecules that inhibit gene expression through the posttranscriptional repression of their target mRNAs, in different pathologic conditions, including renal pathophysiology. miR-21 was also shown to play a dynamic role in inflammatory responses and in accelerating injury responses to promote organ failure and fibrosis. Understanding the cellular and molecular bases of miR-21 involvement in the pathogenesis of kidney diseases, including inflammatory reaction, could be crucial for their early diagnosis. Moreover, the possibility of influencing miR-21 level by specific antagomirs may be considered as an approach for treatment of renal diseases.
Insights
MicroRNA-21 (miR-21) significantly contributes to kidney fibrosis and inflammation by regulating gene expression. Targeting miR-21 may offer a novel therapeutic strategy for chronic kidney diseases.
Area of Science:
- Nephrology
- Molecular Biology
- Genetics
Background:
- Renal fibrosis is a common endpoint for chronic kidney diseases, characterized by apoptosis, epithelial-to-mesenchymal transition, and inflammation.
- The transforming growth factor-β1 (TGF-β1)-Smad3 pathway is a key molecular driver of fibrotic kidney disease.
- MicroRNAs (miRNAs) are emerging as critical regulators in various pathological conditions, including renal pathophysiology.
Purpose of the Study:
- To elucidate the role of miR-21 in the pathogenesis of kidney diseases.
- To understand the cellular and molecular mechanisms underlying miR-21's involvement in renal inflammation and fibrosis.
- To explore the potential of targeting miR-21 for therapeutic interventions in renal diseases.
Main Methods:
- Review of existing literature on renal fibrosis, TGF-β1 signaling, and microRNA function.
- Analysis of studies investigating miR-21 expression and function in kidney injury models.
- Exploration of potential therapeutic strategies involving miR-21 modulation.
Main Results:
- miR-21 plays a significant role in inflammatory responses within the kidney.
- miR-21 accelerates injury responses, contributing to organ failure and fibrosis.
- The expression and activity of miR-21 are closely linked to the progression of renal fibrosis.
Conclusions:
- Understanding miR-21's role in kidney disease pathogenesis is crucial for early diagnosis.
- Modulating miR-21 levels, potentially using antagomirs, represents a promising therapeutic avenue for renal diseases.
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