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Table 1 Differentially expressed genes with greatest absolute log fold changes

From: Natural genetic variation of the cardiac transcriptome in non-diseased donors and patients with dilated cardiomyopathy

  

P value

Adjusted P value

Log fold change

DCM associated

TBX20 target

CMP associated

Comments

Gene symbol

Description

NPPA

Natriuretic peptide A

5.61E-09

2.38E-08

0.58

Yes

No

Yes

Natriuretic factor A and B are used as markers of heart failure progression. Natriuretic factor implicated in development and marker of heart failure, also target of T-box factors [27,28,29,30]

NPPB

Natriuretic peptide B

1.79E-06

5.57E-06

0.57

Yes

Yes

Yes

See NPPA

TBX20

T-box 20

2.87E-25

3.01E-23

0.49

Yes

No

Yes

TBOX20 has been associated with the pathophysiology of DCM in both animal models and human tissue [82] Furthermore, mutations in TBX20 are associated with familial DCM [83, 84]

MYLK3

Myosin light chain kinase 3

1.07E-21

3.15E-20

0.42

Yes

No

Yes

Associated with stress adaptation and progression to heart failure [85,86,87]

CLIC5

Chloride intracellular channel 5

2.88E-26

5.40E-24

0.38

No

No

No

CLIC5 is a member of the family of intracellular Ca2+ channels, associated with the actin cytoskeletal system. Thus far no link with DCM has been described

TRIM44

Tripartite motif containing 44

4.51E-28

3.73E-25

0.38

No

No

No

Thus far no link with DCM has been described

MAVS

Mitochondrial antiviral signaling protein

5.05E-25

4.67E-23

0.36

No

No

No

Thus far no link with DCM has been described

NPR3

Natriuretic peptide receptor 3

3.68E-23

1.68E-21

0.36

No

No

Yes

NPR3 is the receptor for natriuretic peptides in the heart; it is therefore a candidate for studies into the modulation of NPs in (DCM-related) heart failure [88].

SMCR8

Smith-Magenis syndrome chromosome region, candidate 8

3.66E-28

3.46E-25

0.34

No

No

No

Thus far no link with DCM or the heart has been described

JAK2

Janus kinase 2

2.45E-22

8.67E-21

0.32

No

Yes

Yes

JAK2/STAT3 signaling is, amongst other processes, involved myocardial infarction/reperfusion injury, and hypertrophic remodeling in mice. Thus far no direct link with DCM has been described [89]

TUBA3D

Tubulin alpha 3d

1.66E-08

6.63E-08

-0.26

No

No

No

Thus far no link with DCM or the heart has been described

GADD45B

Growth arrest and DNA damage inducible beta

1.43E-08

5.75E-08

-0.27

No

No

Yes

Changes in expression of GADD45B are observed in MI induced HF [90]

DLK1

Delta like non-canonical Notch ligand 1

9.83E-09

4.03E-08

-0.28

No

No

No

Thus far no link with DCM or the heart has been described

TUBA3E

Tubulin alpha 3e

1.17E-10

6.04E-10

-0.30

No

No

No

Thus far no link with DCM or the heart has been described

GADD45G

Growth arrest and DNA damage inducible gamma

2.87E-11

1.58E-10

-0.31

No

Yes

Yes

Gadd45g overexpression promotes heart failure and cardiac remodeling after MI; while knockout mice are resistant to heart failure [91]

RASD1

Ras related dexamethasone induced 1

3.32E-07

1.14E-06

-0.32

No

No

No

RASD1 may be involved in the cardiac release of ANF and BNP upon atrial volume overload in rats [92]. The RASD1 locus is associated with coronary artery disease in human GWAS [93]

MYL7

Myosin light chain 7

8.29E-10

3.89E-09

-0.33

No

No

No

Thus far no link with DCM has been described

FOS

Fos proto-oncogene, AP-1 transcription factor subunit

5.58E-08

2.09E-07

-0.33

No

Yes

Yes

c-FOS is used as a marker of heart failure [94]

MYH6

Myosin heavy chain 6

2.12E-09

9.50E-09

-0.34

Yes

Yes

Yes

MYH6 mutations are associated with familial DCM [95]

DHRS7C

Dehydrogenase/reductase 7C

3.31E-09

1.45E-08

-0.39

No

No

Yes

Decrease of DHRS7C is observed in mouse models of heart failure and in human cardiac tissue of heart failure patients [96, 97]