Mechanisms and inhibitors of ferroptosis in psoriasis

Abstract

Psoriasis is a chronic inflammatory skin disease that features localized or widespread erythema, papules, and scaling. It is common worldwide and may be distributed throughout the whole body. The pathogenesis of psoriasis is quite complex and the result of the interplay of genetic, environmental and immune factors. Ferroptosis is an iron-dependent programmed death that is different from cell senescence, apoptosis, pyroptosis and other forms of cell death. Ferroptosis involves three core metabolites, iron, lipids, and reactive oxygen species (ROS), and it is primarily driven by lipid peroxidation. Ferrostatin-1 (Fer-1) is an effective inhibitor of lipid peroxidation that inhibited the changes related to ferroptosis in erastin-treated keratinocytes and blocked inflammatory responses. Therefore, it has a certain effect on the treatment of psoriatic lesions. Although ferroptosis is closely associated with a variety of human diseases, such as inflammatory diseases, no review has focused on ferroptosis in psoriasis. This mini review primarily focused on the pathogenesis of psoriasis, the mechanisms of ferroptosis, the connection between ferroptosis and psoriasis and ferroptosis inhibitors in psoriasis treatment. We discussed recent research advances and perspectives on the relationship between ferroptosis and psoriasis.

Nanoparticle‐Based MRI‐Guided Tumor Microenvironment Heating via the Synergistic Effect of Ferroptosis and Inhibition of TGF‐β Signaling

“…DFO is an iron chelator that inhibits ferroptosis by reducing the intracellular iron content; [ 31 ] while Fer‐1 can inhibit ferroptosis by impairing lipid peroxidation through upregulation of GPX4 and nuclear factor erythroid 2‐related factor 2. [ 32 ] As shown in Figure 4B,C and Figure S2A,B, Supporting Information, both DFO and Fer‐1 significantly decreased the cytotoxicity of FG‐SR and FG‐STR in MC38 and B16F10 cells. Moreover, TEM revealed that compared with the control group (serum‐free medium, Figure 4D), MC38 cells in the FG‐STR‐treated group exhibited mitochondrial volume reduction with enhanced mitochondrial membrane density and disappearance of mitochondrial cristae, which were reported to be the morphological characteristics of mitochondria during erastin‐induced ferroptosis.…”

Hybrid Biomimetic Membrane Coated Particles-Mediated Bacterial Ferroptosis for Acute MRSA Pneumonia

“…These results showed that GSH At present, the process of ferroptosis is blocked mainly from four aspects: complexation of phosphate with Fe 2+ , chelation with Fe 2+ , antioxidation, and antiferroptosis. 42,43 Iron is among the most active minerals in soil and sediment, which has a strong adsorption capacity for inorganic and organic phosphate compounds. 44 Adenosine triphosphate (ATP), adenosine diphosphate (ADP), and tris(2-carboxyethyl) phosphine (TCEP) have been proved to be able to adsorb iron, resulting in a deficiency of iron, which is indispensable in ferroptosis, and thereby inhibiting ferroptosis and weakening the bactericidal effect.…”

Ferroptosis in lymphoma: Emerging mechanisms and a novel therapeutic approach

“…Ferroptosis is driven by increased cellular iron load and is characterized by the loss in membrane integrity and changes in mitochondrial ultrastructure, including reduced mitochondrial volume, increased mitochondrial bilayer membrane density, decreased mitochondrial cristae, and ruptured mitochondrial membrane ( Doll et al, 2017 ; Du et al, 2022 ; Zhou et al, 2022 ). Ferroptosis can be induced through the interaction of iron regulation, lipid metabolism, and ROS biology, and research in these fields is expected to deepen the mechanistic understanding, biological significance, and clinical therapeutic relevance of ferroptosis ( Table 1 ).…”