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HDAC inhibitors in experimental liver and kidney fibrosis
Katrien Van Beneden1, Inge Mannaerts2, Marina Pauwels1
1Department of Human Anatomy, Liver Cell Biology Lab, Vrije Universiteit Brussel, Brussels, Belgium.
Abstract:
Histone deacetylase (HDAC) inhibitors have been extensively studied in experimental models of cancer, where their inhibition of deacetylation has been proven to regulate cell survival, proliferation, differentiation and apoptosis. This in turn has led to the use of a variety of HDAC inhibitors in clinical trials. In recent years the applicability of HDAC inhibitors in other areas of disease has been explored, including the treatment of fibrotic disorders. Impaired wound healing involves the continuous deposition and cross-linking of extracellular matrix governed by myofibroblasts leading to diseases such as liver and kidney fibrosis; both diseases have high unmet medical needs which are a burden on health budgets worldwide. We provide an overview of the potential use of HDAC inhibitors against liver and kidney fibrosis using the current understanding of these inhibitors in experimental animal models and in vitro models of fibrosis.
Insights
Histone deacetylase (HDAC) inhibitors show promise for treating liver and kidney fibrosis by regulating cell processes. Research explores their potential in preclinical models for these fibrotic disorders.
Area of Science:
- Pharmacology
- Oncology
- Fibrosis Research
Background:
- Histone deacetylase (HDAC) inhibitors are established in cancer therapy, regulating cell survival, proliferation, differentiation, and apoptosis.
- Their therapeutic potential is increasingly explored beyond cancer, including in fibrotic disorders.
- Liver and kidney fibrosis represent significant unmet medical needs with substantial global health economic burdens.
Purpose of the Study:
- To provide an overview of the potential application of HDAC inhibitors in treating liver and kidney fibrosis.
- To summarize current understanding from experimental animal and in vitro models of fibrosis.
Main Methods:
- Review of existing literature on HDAC inhibitors in cancer and fibrotic models.
- Analysis of preclinical data from experimental animal models of liver and kidney fibrosis.
- Evaluation of in vitro studies investigating HDAC inhibition in fibrotic processes.
Main Results:
- HDAC inhibitors demonstrate regulatory effects on key cellular processes relevant to fibrosis.
- Preclinical studies suggest a potential role for HDAC inhibitors in mitigating fibrotic progression.
- In vitro models indicate mechanisms by which HDAC inhibition could counteract fibrotic signaling.
Conclusions:
- HDAC inhibitors represent a promising therapeutic strategy for liver and kidney fibrosis.
- Further research and clinical trials are warranted to validate their efficacy in fibrotic diseases.
- Targeting HDACs could offer novel treatment avenues for patients suffering from liver and kidney fibrosis.
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