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Therapeutic strategies to halt renal fibrosis
Ling Yu1, Nancy A Noble, Wayne A Border
1Fibrosis Research Laboratory, Division of Nephrology, University of Utah, 391 Chipeta Way, Salt Lake City, Utah, UT 84108, USA.
Abstract:
Angiotensin II blockade has become a standard anti-fibrotic therapy in renal diseases because it slows progression to end-stage renal disease. However, current data support the notion that angiotensin II blockade alone cannot stop progressive fibrotic disease. Of an increasing number of therapies showing efficacy in animal studies, antibodies to transforming growth factor beta are the most thoroughly studied and are likely to be effective in human clinical trials. However, hints exist in the literature suggesting that no single agent will effectively halt renal fibrosis and that combinations of agents will be required.
Insights
Angiotensin II blockade slows kidney disease progression but cannot halt fibrosis alone. Combining therapies, like antibodies to transforming growth factor beta, may be necessary to effectively treat renal fibrosis.
Area of Science:
- Nephrology
- Fibrosis Research
- Translational Medicine
Background:
- Angiotensin II blockade is a standard therapy for slowing renal disease progression.
- Current treatments are insufficient to halt progressive renal fibrosis.
- Emerging therapies show promise in preclinical models.
Purpose of the Study:
- To evaluate the efficacy of single-agent therapies for renal fibrosis.
- To explore the potential of combination therapies for halting renal fibrosis.
- To assess the role of transforming growth factor beta antibodies in treating kidney fibrosis.
Main Methods:
- Review of existing literature on anti-fibrotic therapies.
- Analysis of data from animal studies on renal fibrosis.
- Assessment of potential for human clinical trials.
Main Results:
- Angiotensin II blockade alone does not stop progressive renal fibrosis.
- Antibodies to transforming growth factor beta are a promising therapeutic strategy.
- No single agent is likely to be sufficient to halt renal fibrosis.
Conclusions:
- Combination therapies are likely required to effectively halt renal fibrosis.
- Further research into combination anti-fibrotic strategies is warranted.
- Translational studies are needed to confirm efficacy in human trials.