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组蛋白去乙酰化酶:特发性肺纤维化的潜在治疗靶点。

Histone deacetylases: potential therapeutic targets for idiopathic pulmonary fibrosis.

作者信息

Cheng Hai-Peng, Jiang Shi-He, Cai Jin, Luo Zi-Qiang, Li Xiao-Hong, Feng Dan-Dan

机构信息

Department of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.

Hunan Clinical Medical Research Center for Cancer Pathogenic Genes Testing and Diagnosis, Changsha, Hunan, China.

出版信息

Front Cell Dev Biol. 2024 Aug 13;12:1426508. doi: 10.3389/fcell.2024.1426508. eCollection 2024.

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive disease of unknown origin and the most common interstitial lung disease. However, therapeutic options for IPF are limited, and novel therapies are urgently needed. Histone deacetylases (HDACs) are enzymes that participate in balancing histone acetylation activity for chromatin remodeling and gene transcription regulation. Increasing evidence suggests that the HDAC family is linked to the development and progression of chronic fibrotic diseases, including IPF. This review aims to summarize available information on HDACs and related inhibitors and their potential applications in treating IPF. In the future, HDACs may serve as novel targets, which can aid in understanding the etiology of PF, and selective inhibition of single HDACs or disruption of HDAC genes may serve as a strategy for treating PF.

摘要

特发性肺纤维化(IPF)是一种病因不明的慢性进行性疾病,也是最常见的间质性肺疾病。然而,IPF的治疗选择有限,迫切需要新的治疗方法。组蛋白脱乙酰酶(HDACs)是参与平衡组蛋白乙酰化活性以进行染色质重塑和基因转录调控的酶。越来越多的证据表明,HDAC家族与包括IPF在内的慢性纤维化疾病的发生和发展有关。本综述旨在总结关于HDACs及其相关抑制剂的现有信息,以及它们在治疗IPF中的潜在应用。未来,HDACs可能成为新的靶点,有助于理解PF的病因,选择性抑制单个HDACs或破坏HDAC基因可能成为治疗PF的一种策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/566b/11347278/ca03568a6d73/fcell-12-1426508-g001.jpg

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