TABLE 3.

TFs potentially regulating the expression of 316 DE-NMGenes.

#TF	NES	#Targets	Function in pathological hypertrophy
ATF4 (Activating Transcription Factor 4)	6.73	21	–
BACH1	5.27	101	Deletion of BACH1 caused significant reductions in left ventricular hypertrophy (Mito et al., 2008).
NFYA (Nuclear Transcription Factor Y Subunit Alpha)	4.77	75	–
PBX3 (PBX Homeobox 3)	4.45	145	–
NFYC (Nuclear Transcription Factor Y Subunit Gamma)	4.34	117	–
ATF3	4.32	46	Ectopic expression of ATF3 was sufficient to promote cardiac hypertrophy (Koren et al., 2013).
XBP1	3.98	43	Myocardial XBP1s protein was significantly increased in hypertrophic and failing heart (Duan et al., 2016).
KLF4	3.63	45	Overexpression of KLF4 in neonatal rat ventricular myocytes inhibits cardiomyocyte hypertrophy (Liao et al., 2010).
MEF2C	3.54	91	MEF2C silencing attenuated load-induced left ventricular hypertrophy by modulating mTOR/S6K pathway in mice (Pereira et al., 2009).
GATA1 (GATA Binding Protein 1)	3.37	19	–
JUND	3.27	15	JUND could attenuate phenylephrine-mediated cardiomyocyte hypertrophy by negatively regulating AP-1 transcriptional activity (Hilfiker-Kleiner et al., 2006).
IRF2 (Interferon Regulatory Factor 2)	3.27	34	–
MYBL2 (MYB Proto-Oncogene Like 2)	3.27	90	–
MYC	3.17	17	MYC overexpression could induce cardiac hypertrophy (Olson et al., 2013).
GATA5 (GATA Binding Protein 5)	3.14	13	–
RARA (Retinoic Acid Receptor Alpha)	3.12	9	–
YY1	3.02	39	YY1 could prevent cardiac hypertrophy (Sucharov et al., 2008)and suppresses dilated cardiomyopathy and cardiac fibrosis (Tan et al., 2019).

#TFs regulating DE-NMGenes are showed. TFs already proved to play important roles in pathological hypertrophy are marked in bold.