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Table 3 Mechanisms and clinical value of histone modification in keloid

From: Epigenetic modification mechanisms involved in keloid: current status and prospect

Histone modification classification Inhibitor Target Mechanism Clinical value Ref
Histone acetylation N/A N/A N/A N/A  
Histone deacetylation CUDC-907 HDACs CUDC-907 inhibited cell proliferation, migration, invasion, and ECM deposition in KFs and also disrupted the capillaries of keloid explants ex vivo and in vivo A candidate drug for systemic keloid therapy [59]
Histone deacetylation TSA HDACs TSA could also cause abrogation of TGF-β1 induced collagen synthesis and induce apoptosis of proliferating KFs TSA might increase the sensitivity of keloid to radiotherapy and become primary or adjunctive agents for the management of keloid [60]
Histone deacetylation TSA HDACs TSA-induced miR-30a-5p regulated apoptosis and proliferation of keloid fibroblasts via targeting BCL2 A potential use for TSA as effective therapeutic strategies for keloids [62]
  1. HATs and HDACs are able to remove and add acetyl groups to histones, respectively, in this manner emerging as important means of gene regulation. It reveals the precise molecular mechanisms of HDACs inhibitors for clinical keloid treatment. HATs histone acetyltransferases, HDACs histone deacetylases