Abstract
Cell death is essential for the normal metabolism of human organisms. Ferroptosis is a unique regulated cell death (RCD) mode characterized by excess accumulation of iron-dependent lipid peroxide and reactive oxygen species (ROS) compared with other well-known programmed cell death modes. It has been currently recognized that ferroptosis plays a rather important role in the occurrence, development, and treatment of traumatic brain injury, stroke, acute kidney injury, liver damage, ischemia–reperfusion injury, tumor, etc. Of note, ferroptosis may be explained by the expression of various molecules and signaling components, among which iron, lipid, and amino acid metabolism are the key regulatory mechanisms of ferroptosis. Meanwhile, tumor cells of hematological malignancies, such as leukemia, lymphoma, and multiple myeloma (MM), are identified to be sensitive to ferroptosis. Targeting potential regulatory factors in the ferroptosis pathway may promote or inhibit the disease progression of these malignancies. In this review, a systematic summary was conducted on the key molecular mechanisms of ferroptosis and the current potential relationships of ferroptosis with leukemia, lymphoma, and MM. It is expected to provide novel potential therapeutic approaches and targets for hematological malignancies.
Highlights
Death is the common end of all life—from organisms to cells
iron regulatory protein (IRP) can adjust the expression of proteins that may affect the movement of intracellular iron ions into and out of cells [transferrin receptor 1 (TFR1), divalent metal transporter 1 (DMT1), ferroportin (FPN) [32]], storage (FTH), and utilization according to iron metabolism in cells [33]
System Xc, an important antioxidant system, is an amino acid anti-transporter located in the cell membrane and comprises a heterodimer composed of two subunits, i.e., solute carrier family 3 member 2 (SLC3A2) and solute carrier family 7 member 11 (SLC7A11) [56, 57]
Summary
Death is the common end of all life—from organisms to cells. The growth, development, balance, and stability of living organisms depend fundamentally on the organic balance of cell survival and cell death. Ferroptosis is a newly discovered form of irondependent RCD induced by small molecules such as erastin [2] and Ras-selective lethal small molecule 3 [RSL3 [3]], as proposed by Dixon et al [4] in 2012 It exhibits unique morphological, biochemical, and genetic features, which is different from those of the traditional form of cell death [4, 5]. Genetically speaking, ferroptosis is a biological process regulated by multiple genes It generally involves genetic changes in iron homeostasis and lipid peroxidation metabolism. It highlights the importance of further investigation on corresponding underlying specific regulatory mechanisms [9]. Our study is expected to provide a comprehensive understanding of ferroptosis and shed light on the development of novel therapeutic strategies for hematological malignancies
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