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Abstract

Application and Research Progress of Histone Deacetylase Inhibitors in Pulmonary Fibrosis

Author(s): Qian Zhang* and P. Jiang
Department of Respiratory and Critical Care Medicine, The First Central Hospital Affiliated to Nankai University, Nankai, Tianjin 300052, China

Correspondence Address:
Qian Zhang, Department of Respiratory and Critical Care Medicine, The First Central Hospital Affiliated to Nankai University, Nankai, Tianjin 300052, China, E-mail: jenna9898@163.com


Idiopathic pulmonary fibrosis is a fatal and irreversible lung disease with limited therapeutic options. It has always been a difficult problem that we cannot overcome and there is a need for new therapies in clinical treatment. More and more experimental data suggests that the histone deacetylase family of transcriptional corepressors has emerged as crucial mediators of idiopathic pulmonary fibrosis pathogenesis. In order to clarify the role of histone deacetylase inhibitors in pulmonary fibrosis, we searched the database for relevant literatures on histone deacetylase inhibitors and pulmonary fibrosis, and summarized the latest literatures. Epigenetic regulation, such as histone modification and deoxyribonucleic acid methylation, plays an increasingly important role in idiopathic pulmonary fibrosis. Through the regulation of histone modification, we can affect the occurrence and development of idiopathic pulmonary fibrosis. Histone deacetylases not only participates in the development of tumor, but also they are proved to be related to the progress of organ fibrosis. Histone deacetylase inhibitors affect the development of protein function by changing the acetylation level of histone or non-histones. At present, histone deacetylase inhibitors and gene transcription are mostly used in the treatment of skin lymphoma. Many studies have shown that there is a common signal pathway in the occurrence of tumor and lung fiber. By summarizing the literature, upregulated histone deacetylase activities are observed in fibrotic diseases involving the heart, liver, kidneys and lungs. We suggest the significant imbalance of histone deacetylase activity in the onset and progression of idiopathic pulmonary fibrosis lungs. Therefore, the role of histone deacetylase inhibitors in pulmonary fibrosis needs a new understanding and we have also supported histone deacetylase inhibitors in targeting class I histone deacetylase activity in fibroblasts as a therapeutic option and a promising field for idiopathic pulmonary fibrosis patients.

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