Contribution of histone deacetylases (HDACs) to the regulation of histone and non-histone proteins: implications for fibrotic diseases
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Histone deacetylases (HDACs) are essential enzymes that playa pivotal role in the epigenetic regulation of gene expressionby catalyzing the removal of acetyl groups from histone andnon-histone proteins. This deacetylation is a crucial post-translationalmodification that influences several cellular processes,such as chromatin remodeling, transcriptional repression, andsignal transduction. Recent studies have illuminated the significantinvolvement of HDACs in the pathogenesis of fibroticdiseases, conditions characterized by the excessive accumulationof extracellular matrix components leading to progressive organdysfunction and failure. These diseases commonly affect theliver, kidney, heart, lung, and colon. The contribution of HDACsto fibrogenesis is multifaceted, involving the modulation of geneexpression that governs inflammatory and fibrotic signalingpathways. Therefore, targeting HDACs with specific inhibitorshas emerged as a promising therapeutic strategy to mitigatefibrosis in various organs. HDAC inhibitors (HDACi) can potentiallyreverse the aberrant gene expression profiles associatedwith fibrotic diseases by restoring acetylation levels,thus attenuating fibrotic responses. Several HDAC inhibitors,such as vorinostat, trichostatin A, and romidepsin, have shownefficacy in preclinical models of fibrosis, demonstrating theirpotential to suppress fibrogenic signaling pathways and reduceextracellular matrix deposition. In this review, we provide a proteins, and their implications for fibrotic diseases. We comparethe molecular mechanisms by which different classes of HDACscontribute to fibrosis in various organs, and highlight the therapeuticpotential of HDAC inhibition. This review underscoresthe importance of further research into HDAC-specific inhibitorsas viable treatments for fibrotic diseases, aiming to developtargeted therapies that can effectively ameliorate fibrosis andimprove patient outcomes. comprehensive analysis of the current understanding of theroles of HDACs in the regulation of histone and non-histone
Abstract
Histone deacetylases (HDACs) are essential enzymes that playa pivotal role in the epigenetic regulation of gene expressionby catalyzing the removal of acetyl groups from histone andnon-histone proteins. This deacetylation is a crucial post-translationalmodification that influences several cellular processes,such as chromatin remodeling, transcriptional repression, andsignal transduction. Recent studies have illuminated the significantinvolvement of HDACs in the pathogenesis of fibroticdiseases, conditions characterized by the excessive accumulationof extracellular matrix components leading to progressive organdysfunction and failure. These diseases commonly affect theliver, kidney, heart, lung, and colon. The contribution of HDACsto fibrogenesis is multifaceted, involving the modulation of geneexpression that governs inflammatory and fibrotic signalingpathways. Therefore, targeting HDACs with specific inhibitorshas emerged as a promising therapeutic strategy to mitigatefibrosis in various organs. HDAC inhibitors (HDACi) can potentiallyreverse the aberrant gene expression profiles associatedwith fibrotic diseases by restoring acetylation levels,thus attenuating fibrotic responses. Several HDAC inhibitors,such as vorinostat, trichostatin A, and romidepsin, have shownefficacy in preclinical models of fibrosis, demonstrating theirpotential to suppress fibrogenic signaling pathways and reduceextracellular matrix deposition. In this review, we provide a proteins, and their implications for fibrotic diseases. We comparethe molecular mechanisms by which different classes of HDACscontribute to fibrosis in various organs, and highlight the therapeuticpotential of HDAC inhibition. This review underscoresthe importance of further research into HDAC-specific inhibitorsas viable treatments for fibrotic diseases, aiming to developtargeted therapies that can effectively ameliorate fibrosis andimprove patient outcomes. comprehensive analysis of the current understanding of theroles of HDACs in the regulation of histone and non-histone