Epigenetic therapy targeting bone marrow mesenchymal stem cells for age-related bone diseases

Table 2 Histone modification and enzyme mechanism

Enzyme	Histone modification		Heterochromatin	Gene expression	Promoting osteogenesis	References
Enzyme	Sites	Types	Heterochromatin	Gene expression	Promoting osteogenesis	References
G9a SUV39h1/2	H3K9	Methylation	Stable	Down	↑ ↓	[37] [41]
KDM4B	H3K9	Demethylation	Unstable	Up	↑	[39]
EZH2	H3K27	Methylation	Stable	Down	↓	[42]
KDM6B	H3K27	Demethylation	Unstable	Up	–
/	H3K4	Methylation	Unstable	Up	–
KDM5A Jarid1a LSD1	H3K4	Demethylation	Stable	Down	↓ ↓ ↓	[46] [48] [47]
GCN5	H3K9	Acetylation	–	Up	↑	[40]
KAT7	H3K14	Acetylation	–	Up	–	[45]
HDAC1/2	H2A H2B H3 H4	Deacetylation	Stable	Down	↓	[50, 86, 87]

Histone modification enzymes mediate histone methylation, acetylation, and other modification types in different sites. Active modifications can enable the DNA chain to unwind more easily and promote gene expression, while inhibitory modification can compress heterochromatin and inhibit gene expression. Active modification of age-related genes will accelerate BMSC aging and suppress osteogenesis, and active modification of anti-aging genes is carried out to promote osteogenesis and decelerate senescence; inhibitory modification, vice versa
G9a, a lysine-specific histone methyltransferase; SUV39H, a lysine-specific histone methyltransferase; KDM, lysine-specific demethylase; EZH, enhancer of zeste homolog; Jarid1a, Jumonji AT-rich interactive domain 1a; LSD, also known as KDM, lysine-specific demethylase; GCN, also known as Eif2ak4, eukaryotic translation initiation factor 2 alpha kinase 4; KAT7, a histone acetyltransferase; HDAC, histone deacetylase

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