Table 2.
Ferroptosis involvement in the pathological progression of CHD.
| Histological type | Interventions | Features or changes | Pathways or signals | References |
|---|---|---|---|---|
| Vascular endothelial damage | Knock out FPN genes | Increase NTBI, induce chronic iron overload, increase vascular oxidative stress levels, promote AS | [28] | |
| High sugar and high lipid diet | Iron overload, elevated ROS level, downregulation of GPX4 and lipid peroxidation | HMOX1 increase | [57] | |
| PDSS2 | Inhibit VEC ferroptosis and AS progression | Nrf2 activation | [58] | |
| miR-17-92 overexpression | Reduce erastin-induced growth inhibition and ROS generation of HUVEC | A20-ACSL4 axis | [59] | |
| Fluvastatin | Reverse ox-LDL-induced decreases in GPX4 and xCT levels | Regulate GPX4 and xCT | [60] | |
| PM2.5 | Increase ROS production and iron content, decrease GSH, GSH-Px, and NADPH levels, promote lipid peroxidation | [40] | ||
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| ||||
| Arterial wall plaque stability damage | High-iron diet | Iron overload, accelerate inflammation and the formation of macrophage-derived foam cells | [61] | |
| Macrophage-specific FPN1 deficiency | Iron overload, increase oxidative stress and systemic inflammation levels, inhibit ABC transporter protein expression, increase numbers of macrophages, decrease collagen | Downregulate LXRα expression | [62] | |
| High levels of uric acid | Induce the formation of macrophage-derived foam cells and lipid peroxidation | Nrf2/SLC7A11/GPX4 signaling pathway | [63] | |
| Cigarette smoke extract | Increase PTGS2 expression, GSH depletion, and lipid peroxidation, SMC ferroptosis | [64] | ||
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| CM death | Models of HF after MI | Downregulate FTH levels, increase oxidative stress and free iron levels, decrease CM viability | [14] | |
| Erastin, isoprenaline | Increase free iron levels, promote lipid peroxidation, and decrease CM viability | [65] | ||
| Fer-1, puerarin | Inhibit ferroptosis, reduce the loss of CMs | Upregulate the expression of GPX4 and FTH1 | [65] | |
| MI models | Downregulate the levels of GPX4 protein and GPX4 mRNA expression, increase CM death | Reduce GPX4 level | [66] | |
| HUCB-MSC exosomes | Inhibit H/R-induced CM ferroptosis, attenuate myocardial injury | miR-23a-3p/DMT1 axis | [13] | |
| Dexmedetomidine | Inhibit ROS production, maintain the structural integrity of mitochondria, inhibit ferroptosis, attenuate myocardial I/R injury | SLC7A11/GPX4 axis | [67] | |
| Propofol | Reduce SOD and iron accumulation, decrease lipid peroxidation levels, and increase the expression of antioxidant enzymes | AKT/P53 signaling pathway | [68] | |
| HF models | Downregulate GPX4 and FTH1 protein levels | TLR4-NOX4 pathway | [69] | |
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| MF | Inject iron dextran | Increase MDA levels, decrease glutathione peroxidase levels, leading to the occurrence of MF | [70] | |
| miR-375-3p | Promote MF due to CM ferroptosis | Downregulate GPX4 | [71] | |
| Dexmedetomidine | Inhibit CM ferroptosis after myocardial I/R, reduce the area of MF | SLC7A11/GPX4 signaling pathway | [67] | |
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| MH | Apelin-13 | Increase iron and ROS levels in mitochondria of CM, induce mitochondrial damage | Induce the expression of SFXN1 and NCOA4 | [72] |
| Knock out xCT | Increase PTGS2, MDA, and ROS levels, exacerbate Ang II-induced MH | Downregulate xCT | [50] | |
| Beclin 1 haploinsufficient | Elevate levels of SLC7A11, GPX4, and NCOA4, promote autophagy and ferroptosis, and exacerbate low ambient temperature-induced MH | [73] | ||