Table 2 Mouse models of SRF modulation at postnatal developmental stage

α-MHC-SRF

E 7.5–8.0

Overexpression of SRF

• Cardiomyopathy

6 to 40 weeks post-birth

[40]

• Cardiomyocyte hypertrophy

• Dilation of 4 chambers

α-MHC-dmSRF

E 7.5–8.0

Hampered dimerization and DNA binding capacity

• Atrial and ventricular chamber dilation

9–12 days post-birth

[41]

• Reduced ventricular wall thickness

• Smaller cardiomyocytes

• Reduced myofibrils

• Dilated cardiomyopathy

α-MHC-Cre SRF KO

Tamoxifen inducible

Knock out of SRF

• Reduced left ventricular contractibility followed by enlargement

10 weeks after tamoxifen treatment

[39]

• Gradual increase in heart size

• Disruption in cardiomyocyte cytoarchitecture

• Dilated cardiomyopathy

SrfF/F

AAV-Cre at P1

Knockout of floxed SRF upon AAV-Cre treatment

• Loss of T-tubule

–

[3]

• Reduction in cardiomyocyte size

• Hampered sarcomeric assembly

• Decreased mitochondrial size

AAV-Cre at P60

• Minor T-tubule defects

–

• Reduction in cardiomyocyte size

• No sarcomeric disorganization