Table 1.
Selected treatments related to glycolytic enzymes and their mechanisms
Enzymes | Related diseases | Treatment | Mechanism | Effects | References |
---|---|---|---|---|---|
Hexokinase | Myocardial infarction | IPC | Phosphorylation of HK2 at Thr-473 via the Akt signaling pathway, thereby increasing HK2 binding to mitochondria | Improved myocardial resistance to mPTP openig and cell death after reperfusion | [16] |
Hexokinase | Myocardial infarction | Low temperature | Similar to IPC | Reduces cardiac energy demand and prevents ischemia–reperfusion injury | [37] |
Hexokinase | Cardiomegaly | PHLPP | Dephosphorylates Akt and reduces the level of HK2 bound to cardiac mitochondria | Associated with the development of cardiac hypertrophy | [51] |
Hexokinase | Ischemia–reperfusion | Resveratrol | Inhibits VDAC1 phosphorylation via the Akt-GSK3β pathway and promotes de-VDAC1 binding to HK2 | Prevention of ischemia–reperfusion injury | [32] |
Hexokinase | Ischemia–reperfusion | Melatonin | It inhibits mitochondrial fission by activating AMPKα | Protects the cardiac microvascular system from IR | [38] |
Hexokinase | Ischemia–reperfusion | TAT-HK2 | Induced HK2 translocation from mitochondria | Exacerbates cardiac reperfusion injury | [41] |
Hexokinase | Heart failure | QXF | Promote the activation of KLF5, which in turn increases the activity of the HK2 gene promoter | Induces glucose metabolism and inhibits cardiomyocyte apoptosis | [52] |
Hexokinase | Heart Failure | Cana | Inhibition of IL-6 release and ERK1/2 phosphorylation by reducing HK2 expression, ultimately leading to reduced inflammation in endothelial cells | Reducing Vascular Inflammation in Heart Failure | [53] |
PFK1 | Heart failure | TIGAR | Increases endothelial glycolytic function | Improves endothelial angiogenesis and thereby improves heart failure | [69] |
Aldolase | Heart Failure | Ginsenoside Rg1 | It regulates the aldolase/AMP-activated protein kinase/PINK1 pathway | Limiting nutritional stress-induced H9c2 cell injury | [201] |
ENO | Heart failure | KS/Serpina3c | Inhibits transcriptional activation of ENO1 by regulating acetylation of Nr4a1, ultimately reducing excessive activation of glycolysis | Prevention of myocardial fibrosis after MI | [117] |
PKM | Myocardial infarction | PCA | Promoting Cy-clin-D1 and C-Myc expression through regulation of the β-linked protein/TCF4 signaling cascade | Reduces heart damage and protects cardiomyocytes from apoptosis | [202] |
PKM | Ischemia–reperfusion | ISB | Targeting PKM2 to reduce macrophage inflammation | Reduces damage caused by I / R | [139] |
PKM | Heart failure | TEPP-46、2-DG | Promotes the formation of stable tetramers with high pyruvate kinase activity | It provides a new idea for the treatment of chemotherapy drug-induced heart failure | [148] |
LDH | Cardiomegaly | miR-375-3p inhibitors | Induced LDHB expression | It inhibits Ang II-induced cardiomyocyte hypertrophy | [161] |