A new form of cell death, ferroptosis, was recently discovered and approved to regulate various disease progress (Figure 1). Ferroptosis is an iron-dependent programmed cell death resulting from alterations of metabolic processes and accumulation of lipid peroxidation that is toxic and can disturb the membrane structure. Ferroptosis initiation and execution lies at the intersection of amino acid, lipid, and iron metabolism, but the sensitivity of ferroptosis is also modulated by several lines of mechanisms, including A) the regulation of GSH and redox homeostasis, such as function of system Xc-, GPX4 regulation, FSP1-CoQ10- NAD(P)H pathway, sulfur transfer pathway, mevalonate (MVA) pathway, glutamine metabolic pathway, NRF2 and p53 regulatory axis; B) the regulation of iron homeostasis, such as the regulation of ATG5-ATG7-NCOA4 pathway, IREB regulation system, and the regulatory pathways of heatshock proteins; C) related enzymes around glucose and lipid metabolism, such as PHGDH, G6PD, ACSL4, and LPCAT3, etc. ; D) mitochondria function regulation, such as VDAC, mitochondrial electron transport chain (ETC) , TCA cycle and glutaminolysis.
Here, we provide featured antibodies against key targets of iron homeostasis, redox regulation, GSH homeostasis, and lipid metabolism from ABclonal.
Ferroptosis has played critical roles in various diseases, such as nervous system diseases, heart diseases, liver diseases, gastrointestinal diseases, lung diseases, kidney diseases, pancreatic diseases, and etc (Image adapted from Li, J., Cao, F., Yin, Hl. et al. Ferroptosis: past, present and future. Cell Death Dis 11, 88 (2020)).