Table 2.
Research progress on ferroptosis in acute myeloid leukemia.
| Researcher | Research object | Related Pathway | Target | Conclusions/Results | |
|---|---|---|---|---|---|
| Sarah Weber (110) | Patients/mice | Iron Metabolism pathway | Iron | Iron overexpression in patients with MDS and AML | |
| Eric Grignano (111) | Leukemic cells in vivo experiments/Patients | Iron Metabolism pathway | Iron | Iron overload in AML | |
| Rudy Birsen (112) | AML cells both in vivo and ex vivo | GSH synthesis pathway | System Xc- GPX4 | SLC7A11 or GPX4 genes were inactivated in MDS and AML cells after exposure to APR-246 | |
| Jie Wei (113) | AML patient samples and normal samples | Lipid peroxidation | Glutathione peroxidases (GPXs) | High expression of GPX-1, -3, -4, and -7 in AML patients | |
| Yan Du (114) | AML xenograft mouse model/in vitro studies | Lipid synthesis pathway | ROS | Overexpression of lipid ROS in AML cells due to ATPR | |
| Hai-Yan Zhu (115) | AML cells | Lipid synthesis pathway | ROS | The accumulation of intracellular and mitochondrial ROS and the activation of AMPK in AML due to TYP | |
| Rushdia Zareen Yusuf (116) | Leukemic cells in multiple mouse/human myeloid leukemias | Lipid peroxidation | Glutathione peroxidase-4 (GPX4) | Glutathione peroxidase-4 (GPX4) inhibitors inhibited ALDH3A2 in AML | |
| Fanghua Ye (117) | HL-60/NRAS Q61L cells | The RAS-JNK/p38 pathway | TFR1 | Through the Ras-JNK/p38 pathway, HMGB1 was downregulated and reduced the level of TFR1 in HL-60 cells | |
| Jing Du (118) | AML cell lines | AMPK/mTOR/p70S6k signaling pathway | Ferritin/Iron/ROS | Increased unstable iron and ROS in AML due to DHA | |
| Jessica Sagasser (119, 120) | Leukemia cell lines such as HL-60 cells | Lipid synthesis pathway | ROS | Chloride [N,N'-disalicidene-1,2-phenylenediamine] iron(III) complexes produced, induced lipid ROS and induce ferroptosis in HL-60 cells | |
| Yan Yu (121) | HL-60 cells | Activation of JNK and p38 signaling pathway | HMGB1 release | Erastin increased the sensitivity of AML cells to chemotherapeutic agents. | |
| Li-Hua Dong (122) | AML cell lines(K-562 and HL-60)/ the nude mice/AML patients | The putative binding sites among circKDM4C, hsa-let-7b-5p, and P53 | P53 | CircKDM4C upregulated P53 by sponging hsa-let-7b-5p to induce ferroptosis in AML | |
| Zhe Chen (123) | AML cells | Iron metabolism pathway | Iron | Increased iron ameliorated AML by inducing the death of iron-dependent cancer cells | |