Histone Deacetylase: A Potential Therapeutic Target for Fibrotic Disorders

Pang, Maoyin; Zhuang, Songlin

doi:10.1124/jpet.110.168385

Cited by 162 publications

(147 citation statements)

References 82 publications

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“…To date, there are 18 known HDACs including: class I HDACs [33]; class IIa HDACs [34]; class IIb HDACs [35]; class III HDAC enzymes sirtuins [35]; and finally the only class IV enzyme HDAC11 [33]. To catalyse the deacetylation of histone groups, HDACs together with HDAC related deacetylases, must switch a single metal ion at the metal ion binding site Mn 2+ B in arginase [36].…”

Section: Dna Methylation and Histone Modificationmentioning

confidence: 99%

DNA Methylation in Mammalian Cells

Winata¹,

William²,

Keena³

et al. 2018

Gene Expression and Regulation in Mammalian Cells - Transcription Toward the Establishment of Novel Therapeutics

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Epigenetic regulation was first studied in the 1970s and has quickly gained global interest. It is involved at many different stages of mammalian cell development. The broad nature of epigenetic regulation has led to it being referred to as an 'all stage' mechanism of regulation as it is implicated in many developmental stages including embryonic development, ageing and in cancer progression. The term 'epigenetic' refers to the alteration of gene expression without changing the genomic sequence. Epigenetic regulation involves the main subtypes of DNA methylation and histone modification, and microRNA expression. Epigenetic alteration is used by mammalian cells to 'turn-on and -off' the gene expression. During embryonic development this process is used to induce cell apoptosis of genes that are no longer useful. During cancer development, epigenetics works to repress tumour suppressor gene expression and activate oncogene expression. The stability and sustainability for the detection of epigenetic markers make it an attractive area for biomarker and drug discovery. In this book chapter we will discuss the key epigenetic processes involved in mammalian cell development and disease progression, specifically in cancer.

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Section: Dna Methylation and Histone Modificationmentioning

confidence: 99%

DNA Methylation in Mammalian Cells

Winata¹,

William²,

Keena³

et al. 2018

Gene Expression and Regulation in Mammalian Cells - Transcription Toward the Establishment of Novel Therapeutics

View full text Add to dashboard Cite

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“…[13] CLASSIFICATION OF HDACs [2] Acetylation and deacetylation are structured by two groups of enzymes: HATs (histone acetyltransferases) and HDACs (histone deacetylases).…”

Section: Hdacsmentioning

confidence: 99%

“…Mechanisms include DNA methylation, chromatin histone alterations [1,13] , novel transcripts and functional noncoding RNAs, such as microRNAs and long noncoding RNAs. [1] Post-translational alterations of histone H3, heat shock protein-27 (HSP-27) and mitogenactivated protein (MAP) kinase p38 expression.…”

Section: Mechanisms In Dnmentioning

confidence: 99%

“…[12] NEPHROPATHY AND FIBROSIS [13,40] HDAC activity is also linked with the development and progression of some chronic diseases characterized by fibrosis, including chronic kidney disease, cardiac hypertrophy, and idiopathic pulmonary fibrosis. [13] www.wjpps.com Vol 6, Issue 9, 2017. 348…”

Section: Retinopathy Rolementioning

confidence: 99%

“…STAT3 may mediate those actions of HDACs. [13] Trichostatin A, a nonselective HDAC inhibitor, reduced mRNA and protein expressions of ECM modules and prevented EMT. [10] IV] CURCUMIN [18] Increased levels of HSP-27 and MAP kinase (p38) in diabetic kidney.…”

Section: Omprakash World Journal Of Pharmacy and Pharmaceutical Sciementioning

confidence: 99%

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Embryonic Life of Hdac Inhibitors: – In Diabetic Nephropathy

Soni¹

2017

WJPPS

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Effect of histone deacetylase inhibitor on epithelial‐mesenchymal transition of liver fibrosis

et al. 2018

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Liver fibrosis is an excessively reversible wound healing process and the fibrotic disorder is the activation of hepatic stellate cell that requires extensive alterations in gene expression. As reversible deacetylation of histone proteins modulate gene expression, we examined the effect of valproic acid (VPA) as selective histone deacetylase inhibitor on CCl-4 induced liver fibrosis. Thirty rats were divided into three equal groups; control group, fibrotic group and VPA-treated group. The rats were sacrificed after 6 weeks of liver fibrosis induction. The histopathological effect on liver tissue was examined. The expression of α-SMA and Smad-4 mRNA and serum levels of TGF-β1, alanine aminotransferase, and aspartate aminotransferase were determined. Treatment of rats with VPA attenuated carbon tetrachloride-induced liver fibrosis. Moreover, α-SMA and Smad-4 expression was repressed under VPA treatment and both serum TGF-β1 and liver enzymes were significantly decreased. The histone deacetylase inhibitor-1 VPA inhibits the epithelial-mesenchymal transition and affects hepatic stellate cell activation during liver fibrosis through downregulation of Smad4 and α-SMA expression which may serve as a promising agent in liver fibrosis treatment. © 2018 IUBMB Life, 70(6):511-518, 2018.

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Histone Deacetylase: A Potential Therapeutic Target for Fibrotic Disorders

Cited by 162 publications

References 82 publications

DNA Methylation in Mammalian Cells

DNA Methylation in Mammalian Cells

Embryonic Life of Hdac Inhibitors: – In Diabetic Nephropathy

Effect of histone deacetylase inhibitor on epithelial‐mesenchymal transition of liver fibrosis

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