Table 2.

Results of the relationship between epigenetic factors and lung health in included studies in this systematic literature review

Epigenetic factors	Activity in asthma, COPD, or smoking	Reference	Sample size	Type of sample	Country
Class 1 HDAC Family
HDAC 1	Decreased in asthma, not yet studied in smoking and COPD patients	[27]	40	Bronchial biopsy samples	UK
		[28]	28	Alveolar macrophages	UK
		[29]	24	Rat lung tissue	UK
HDAC 2	Decreased in asthma, smoking and COPD	[27]	40	Bronchial biopsy samples	UK
		[28]	28	Alveolar macrophages	UK
		[29]	24	Rat lung tissue	UK
		[30]	29	Human bronchial biopsies	UK
HDAC 3 and 8	Decreased in COPD, no difference in asthma, limited published data in smoking	[28]	28	Alveolar macrophages	UK
		[31]	159	Human lung tissue	USA and Canada
Class II HDAC family
HDAC 5	Decreased in COPD, no difference in asthma, limited published data in smoking	[28]	28	Alveolar macrophages	UK
		[31]	159	Human lung tissue	USA and Canada
Class III HDAC family
SIRT1	Limited published data
Class IV HDAC family
HDAC 11	Limited published data
GNATs-HAT family
HAT1, GCN5, GCN5L, Elp3, PCAF	Increased in asthma patients, limited published data on smoking and COPD	[27]	40	Bronchial biopsy samples	UK
		[32]	–	Cell culture-mature monocytes	USA
General transcription factor-HATs
TAF250, TFIIIC	Increased in asthma, limited published data on smoking and COPD	[27]	40	Bronchial biopsy samples	UK
		[28]	28	Alveolar macrophages	UK

HDAC, histone deacetylase; SIRT1, sirtuin; HAT, histone acetyl transferase; GCN5, general control of amino acid synthesis protein 5; GCN5L, general control of amino acid synthesis protein 5 ligand; Elp3, elongation complex protein; PCAF, protein300/CREB-binding protein-associated factor; TAF250, TBP-associated factor 250 kDa; TFIIIC, transcription factors IIIC.