|
| Target HDAC or HAT | Molecular pathway | Experimental model | Cardiovascular effect | Reference |
|
| ↑ Sirt1 | ↑ PGC-1α
↑ Bcl2
↓ Bax, caspase 3
↑ SOD, SDH, Cyt-c oxidase | TAC induced myocardial infraction
In vivo
Hypoxia induced dysfunction
In vitro | ↑ LVEF
↓ fibrosis
↓ apoptosis | [52] |
| ↑ Sirt3 | ↓ TGF-β/Smad3 | TAC induced heart failure
In vivo | ↓ fibrosis
↓ collagen deposition
↓ cardiac hypertrophy
Prevented decrease in cardiac FS
Preserved diastolic function | [53] |
| ↑ Sirt1 | ↑ SOD | Chronic heart failure model
In vivo
Ang II or antimycin A induced oxidative stress
In vitro | ↑ FS
↑ LVEF
↑ survival
↓ apoptosis | [54] |
| ↑ Sirt3 | ↑ SOD | Dox-induced mitochondrial dysfunction
In vivo
In vitro | ↓ oxidative stress
↑ ATP mitochondrial production | [32] |
| ↑ Sirt1 | ↓ p38MAPK
↓ caspase 3
↓ Bax
↑ Bcl-2
↑ SOD1 | Dox-induced heart failure
In vivo | ↑ FS
↓ apoptosis
↓ oxidative stress | [55] |
| ↑ Sirt1 | ↑ AMPK | Dox-induced cardiotoxicity
In vitro | ↑ survival | [56] |
| ↑ Sirt3 | ↓ p53
↓ Bax, Cyt-c | Dox-induced cardiotoxicity
In vivo | ↓ apoptosis
Attenuated loss of diastolic and systolic function. | [57] |
| ↑ Sirt1 | ↓ USP7
↓ p300
↓ Bax, caspase 3
↓ p53 | Dox-induced cardiotoxicity in young and aged hearts
In vivo | ↑ FS
↑ EF
↓ LVEDS
↓ apoptosis | [58] |
| ↑ Sirt1 | ↑ PI3K-Akt
↓ TNF-α
↓ FAS/FADD/caspase 8
↓ caspase 3
↑ FoxO3 | Exercise during aging
In vivo | ↑ FS
↓ fibrosis
↓ apoptosis | [41] |
| ↑ Sirt1 | ↓ ac-FoxO1
↓ Bim, Bax
↓ p53 | Aging
In vivo | ↑ FS
↑ LVEF
↓ fibrosis
↓ apoptosis | [40] |
| ↑ Sirt1 | ↑ SOD
↑ GSH | High glucose-induced mitochondrial oxidative stress.
In vitro | ↓ oxidative stress | [59] |
| ↑ Sirt1 | ↓ p53
↑ SDF-1 | NE-induced hypertrophy
In vitro
Hypertension model
In vivo | ↓ hypertrophy
↑ bioavailable NO
↓ apoptosis | [60] |
In T1DM:
↑ Sirt1, Sirt2, Sirt3, and Sirt5.
In T2DM:
↑ Sirt1 and Sirt2
↓ Sirt3, which was initially elevated | ↓ B-MHC
↓ Akt | T1DM-induced cardiomyopathy
In vivo
T2DM-induced cardiomyopathy
In vivo | In T1DM rats:
↓ cardiac atrophy
In T2DM rats:
↓ cardiac hypertrophy | [61] |
| ↑ Sirt1, Sirt3, Sirt4, and Sirt7 | ↓ caspase 3 | H2O2-induced apoptosis
In vitro | ↓ apoptosis | [62] |
| Most effects abolished when using sirtinol | ↑ SOD1, SOD3, GPx1, catalase.
↓ NOX2, NOX4
↑ GTP cyclohidrolase 1 and biopterin | In vivo
Apo-lipoprotein E Knockout mice | ↓Oxidative stress
Reversed eNOS uncoupling | [63] |
|
