Table 3.

Mechanisms and clinical value of histone modification in keloid

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]

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