Table 2.
The role of ferroptosis in various cardiovascular diseases.
| Diseases | Characteristics or changes | Pathways or signals | References |
|---|---|---|---|
| DIC | Excess lipid peroxides production in mitochondria | Down-regulation of GPX4 expression | Tadokoro et al. (22) |
| DIC | Up-regulation of Hmox1 expression | NRF2/Hmox1 pathway | Fang et al. (23) |
| DCM | Lipid peroxidation | Advanced Glycation end-products (AGEs) inhibited SLC7A11 expression and ferritin, decreased GSH expression and increased unstable iron levels. | Wang et al. (33) |
| Sepsis cardiomyopathy | Iron overload and excessive ROS in mitochondria | NCOA4 expression increased, interacted with ferritin, activated SFXN1 expression, and transferred Fe2+ to mitochondria | Li et al. (35) |
| Diabetic Atherosclerosis | Iron overload, ROS increased, down-regulation of GPX4 and SCL7A11, lipid peroxidation and together resulted in ferroptosis in endothelial cells | Hmox1 increased | Meng et al. (42) |
| AMI | Accumulation of lipid peroxides | Down-regulation of GPX4 | Park et al. (44) |
| AMI | GSH level decreased, iron deposition, Fe2+ level increased, excessive lipid peroxides and ROS | DMT1 overexpression | Song et al. (47) |
| I/RI | Up-regulation of USP7, p53 and TfR1 | USP7 / p53 / TfR1 pathway | Tang et al. (52) |
| I/RI | Mitochondrial dysfunction, calcium transients blocked and contractile dysfunction | Loss of GPX4 activity | Stamenkovic et al. (53) |
| Diabetic I/RI | A increase in myocardial oxidative stress, apoptosis, pyroptosis and ferroptosis | Nox2 activation mediated through AMPK suppression | Wang et al. (59) |
| Diabetic I/RI | The interaction between endoplasmic reticulum stress and ROS caused cardiomyocytes injury | ATF4-CHOP pathway | Li et al. (60) |
| I/RI related to heart transplantation | Neutrophils recruitment to impaired myocardium | TLR4/TRIF pathway | Li et al. (61) |
DIC, doxorubicin-induced cardiomyopathy; GPX4, glutathione peroxidase 4; Hmox1, heme oxygenase-1; NRF2, NF-E2-related factor 2; DCM, Diabetic cardiomyopathy; AGEs, advanced glycation end-products; ROS, reactive oxygen species; NCOA4, nuclear receptor coactivator 4; SFXN1, siderofexin; SCL7A11, solute carrier family 7 member 11; AMI, acute myocardial infarction; GSH, glutathione; DMT1, divalent metal transporter 1; I/RI, ischemia/reperfusion injury; USP7, ubiquitin-specific protease 7; p53, protein 53; TfR1, transferrin receptor 1; Nox2, NADPH oxidase 2; AMPK, AMP-activated protein kinase; ATF4, Activating transcription factor 4;CHOP, C/EBP homologous protein; TLR4, toll-like receptor 4; TRIF, TIR domain-containing adapter-inducing interferon-β.