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2016 ; 23
(3
): 369-79
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Ferroptosis: process and function
#MMPMID26794443
Xie Y
; Hou W
; Song X
; Yu Y
; Huang J
; Sun X
; Kang R
; Tang D
Cell Death Differ
2016[Mar]; 23
(3
): 369-79
PMID26794443
show ga
Ferroptosis is a recently recognized form of regulated cell death. It is
characterized morphologically by the presence of smaller than normal mitochondria
with condensed mitochondrial membrane densities, reduction or vanishing of
mitochondria crista, and outer mitochondrial membrane rupture. It can be induced
by experimental compounds (e.g., erastin, Ras-selective lethal small molecule 3,
and buthionine sulfoximine) or clinical drugs (e.g., sulfasalazine, sorafenib,
and artesunate) in cancer cells and certain normal cells (e.g., kidney tubule
cells, neurons, fibroblasts, and T cells). Activation of mitochondrial
voltage-dependent anion channels and mitogen-activated protein kinases,
upregulation of endoplasmic reticulum stress, and inhibition of cystine/glutamate
antiporter is involved in the induction of ferroptosis. This process is
characterized by the accumulation of lipid peroxidation products and lethal
reactive oxygen species (ROS) derived from iron metabolism and can be
pharmacologically inhibited by iron chelators (e.g., deferoxamine and
desferrioxamine mesylate) and lipid peroxidation inhibitors (e.g., ferrostatin,
liproxstatin, and zileuton). Glutathione peroxidase 4, heat shock protein beta-1,
and nuclear factor erythroid 2-related factor 2 function as negative regulators
of ferroptosis by limiting ROS production and reducing cellular iron uptake,
respectively. In contrast, NADPH oxidase and p53 (especially
acetylation-defective mutant p53) act as positive regulators of ferroptosis by
promotion of ROS production and inhibition of expression of SLC7A11 (a specific
light-chain subunit of the cystine/glutamate antiporter), respectively.
Misregulated ferroptosis has been implicated in multiple physiological and
pathological processes, including cancer cell death, neurotoxicity,
neurodegenerative diseases, acute renal failure, drug-induced hepatotoxicity,
hepatic and heart ischemia/reperfusion injury, and T-cell immunity. In this
review, we summarize the regulation mechanisms and signaling pathways of
ferroptosis and discuss the role of ferroptosis in disease.
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