Table 1 Intervention of Ankrd1 in cardiomyocytes

Physiology

–

H9c2 cells

Overexpression with plasmid

Nonphosphorylatable form of Ankrd1 repressed the promoter activity of MLC-2v

Nonphosphorylatable form of Ankrd1 decreased the cell size of H9c2 cells more efficiently than wild-type Ankrd1

[22]

Physiology

–

H9c2 cells

Overexpression with plasmid

Increased the protein level of p53; decreased the protein level of Mdm2

–

[59]

Physiology

–

H9c2 cells

Overexpression with plasmid

Increased the expression of hypertrophic proteins p-ERK1/2 and p-GATA4

–

[48]

Physiology

–

C57BL/B6 mice

Global deletion of MARP

Normal cardiac morphology and cardiac function; did not change the heart/body weight ratios

–

[41]

Physiology

–

Male mice

Global deletion of Ankrd1

Normal cardiac function

–

[28]

Physiology

–

C57/BL6J mice

Cardiac-specific overexpressing

No physiological abnormalities

–

[47]

Physiology

–

Mice

Cardiac-specific overexpressing

Cardiomyocyte disorganization and myofibrillar disruption

Developed sinus venosus defect and progressive ventricular diastolic dysfunction

[42]

AIC

Doxorubicin

Adult rat ventricular myocytes

Knockdown with siRNA

Inhibited myofilament gene transcription and disrupted cardiomyocyte sarcomere structure; reversed the GATA4 rescue of the doxorubicin-induced sarcomere phenotype

–

[7]

AIC

Doxorubicin

Adult rat ventricular myocytes

Overexpression with adenovirus

Unable to rescue the doxorubicin-induced sarcomere disarray phenotype

–

[7]

DCM

MLP knockout

Sv129/black swiss mice

Global deletion of Ankrd1

Prevented the formation of Ankrd1/PKCα/PLCβ1 complex, and inhibited the accumulation of PKCα at the intercalated discs

Alleviated the DCM phenotype in MLP knockout mice

[29]

DCM

EAM

BALB/c mice

Global deletion of Ankrd1

Mitigated myocarditis-induced cardiac damage/remodeling

–

[50]

HCM

Ang II

NRVCs

Overexpression with adenovirus

Upregulated the expression of ANP, β-MHC and calcineurin

Enhanced Ang II-induced myocyte hypertrophy

[38]

HCM

Ang II

Neonatal rat cardiomyocytes

Overexpression with adenovirus

Enhanced the mitochondrial translocation of Bax and phosphorylated p53, increased mitochondrial permeability and cardiomyocyte apoptosis, and reduced cell viability

–

[60]

HCM

Ang II

Neonatal rat cardiomyocytes

Knockdown with shRNA

Decreased the mitochondrial translocation of Bax and phosphorylated p53, inhibited mitochondrial permeability and cardiomyocyte apoptosis, and increased cell viability

–

[60]

HCM

Isoprenaline

Engineered heart tissue

Overexpression with adenovirus

Did not change the basal force of contraction; decreased the contractile response to Ca⁺ and isoprenaline in engineered heart tissue

–

[37]

HCM

Isoprenaline

C57/BL6J mice

Cardiac-specific overexpressing

Decreased the myocyte area and fibrosis; decreased the left ventricular posterior wall thickness, HW/BW and HW/TL ratios

Inhibited isoprenaline-induced cardiomyocyte hypertrophy

[47]

HCM

Phenylephrine

Neonatal rat cardiomyocytes

Overexpression with adenovirus

Decreased the myocyte area; reduced the expression of the hypertrophic molecular markers α-actin, β-MHC, and ANF; inhibited the MAPK/ERK signaling pathway

Inhibited phenylephrine-induced hypertrophy

[47]

HCM

Phenylephrine

NRVCs

Knockdown with siRNA

Decreased phenylephrine-induced phosphorylation of ERK1/2 and GATA4, inhibited nuclear translocation of the Ankrd1 complex

Inhibited phenylephrine-induced hypertrophy

[28]

HCM

Phenylephrine

Male mice

Global deletion of Ankrd1

–

Inhibited phenylephrine-induced hypertrophy

[28]

HCM

TAC

C57BL/6 male mice

Overexpression with adenovirus

Increased the cytosolic CARP level, the heart weight/body weight ratio, and the expression of calcineurin

–

[38]

HCM

TAC

C57BL/6 male mice

Overexpression with adenovirus

Increased the lung weight/body weight ratio, decreased the left ventricular fractional shortening, increased cardiomyocyte apoptosis and the expression of phosphorylated p53

–

[60]

HCM

TAC

C57BL/6 male mice

Overexpression of nuclear Ankrd1

Induced cardiac remodeling by activating MYH7

–

[18]

HCM

TAC

C57/BL6J mice

Cardiac-specific overexpressing

Decreased the myocyte area and fibrosis; inhibited the decrease in α-MHC and SERCA2 expression induced by TAC; decreased the left ventricular posterior wall thickness and the LV mass; no difference in cardiac function (EF%, FS%); inhibited the MAPK/ERK and TGF-β/Smad3 signaling pathway

Inhibited TAC-induced cardiomyocyte hypertrophy

[47]

HCM

TAC

C57BL/6 male mice

Knockdown with shRNA

–

Inhibited TAC-induced hypertrophy

[38]

HCM

TAC

C57BL/6 male mice

Knockdown with shRNA

Inhibited TAC-induced cardiomyocyte apoptosis and the expression of phosphorylated p53

–

[60]

HCM

TAC

Male mice

Global deletion of Ankrd1

–

Did not affect TAC-induced hypertrophy

[28]

HCM

TAC

C57BL/B6 mice

Global deletion of MARP

–

Did not affect TAC-induced hypertrophy

[41]

ICM

Hypoxia

H9c2 cells

Overexpression with plasmid

Diminished the hypoxia-induced apoptosis

–

[61]

ICM

H/R

Neonatal mouse ventricular cardiomyocytes

Overexpression with adenovirus

Overexpressed Ankrd1 was mainly distributed in the nucleus; increased Bcl-2 gene expression

Decreased H/R-induced apoptosis

[62]

ICM

H/R

Neonatal mouse ventricular cardiomyocytes

Knockdown with shRNA

–

Enhanced H/R-induced apoptosis

[62]