Table 2.
Experimental Model | Intervention | The Effect of Intervention | Reference |
---|---|---|---|
Adult male CD-1 mice with induced cardiac fibrosis | Honokiol | Protects against the appearance and progression of cardiac hypertrophy by activating mitochondrial SIRT3; Honokiol directly binds to SIRT3 and increases its enzymatic activity, affinity for NAD+ and gene expression. |
[124] |
Male Sprague Dawley rats; Transverse aortic constriction (TAC)-induced hypertrophy | Choline | Decreases cardiac hypertrophy and fibroses by activating SIRT3-AMPK-UPRmt signaling; Improves metabolic function; Increases serum beta-hydroxy butyrate and acetylcholine levels; Increases cardiac levels of enzymes required to metabolize ketone bodies and fatty acids that decrease cardiac hypertrophy. |
[125] |
TAC mice models | Sesamin | Decreases cardiac hypertrophy, fibrosis and inflammation; Improves cardiac function; Sesamin-induced reduction in hypertrophy is dependent on SIRT3, which decreases ROS; Increases SIRT3 and SOD2 expression and decreases FOXO3a phosphorylation. |
[126] |
In vitro neonatal rat cardiomyocytes hypertrophy model induced by ANGII | Hydrogen sulfide | ↑ SIRT3 promoter activity and expression; ↓ Hypertrophy, ↑ mt function, ↑ SOD2 and FOXO3a expression, ↓ oxidative stress; All hydrogen sulfide-induced changes were SIRT3-dependent. |
[127] |
Mice with TAC induced hypertrophy | ↓ Cardiac hypertrophy, ↓ ROS, ↓ Blood pressure; Restores myocardial mitochondrial structure, number and volume; ↑ OPA1, MFN1, MFN2 (mitochondrial fusion genes that increase respiratory chain efficiency) and pro PGC-1α, all the modifications being SIRT3 dependent. |
[127] | |
Mice with TAC induced hypertrophy | Dihydromyricetin | ↓ Hypertrophy, ↓ ROS, ↑ expression and activity of SIRT3, FOXO3a, SOD2; Activates AMPK-PGC1alpha-ERRalpha axis, which increases SIRT3 expression and leads to mtSOD2 deacetylation and decreased oxidative damage. |
[128] [129] |
Resveratrol | ↓ Cardiac hypertrophy and collagen deposition, ↑ Cardiac function, all in an SIRT3-dependent manner; In vitro, prevents fibroblast-myoblast differentiation by inhibiting TGFbeta-Smad3 signaling. |
[130] | |
NAD+ | ↓ Hypertrophy in a SIRT3-dependent manner by activating SIRT3-LKB1-AMPK signaling and culminates with decreased mTOR activity and decreased hypertrophy; Pathologic cardiac hypertrophy decreases Nampt and NAD+ levels (but not in exercise-induced hypertrophy). |
[131] | |
Emodin | ↑ PGC-1α-SIRT3 signaling. | [132] | |
Angiotensin II induced hypertrophy in cardiomyoblast H9c2 cells | 1,25-OH vitamin D3 | ↓ Hypertrophy in a SIRT3 independent manner; SIRT3 expression was unaffected by the intervention. |
[133] |
Abbreviations: ↑ increases, ↓ decreases.