Transcription factors in ferroptotic cell death

Dai, Chongshan; Chen, Xin; Li, Jingbo; Comish, Paul B.; Kang, Rui; Tang, Daolin

doi:10.1038/s41417-020-0170-2

Cited by 171 publications

(136 citation statements)

References 96 publications

Supporting

Mentioning

136

Contrasting

Order By: Relevance

“…Cells that undergo ferroptosis exhibit a typical necrotic morphology and dysmorphic mitochondrial phenotype, including shrunken mitochondria, increased mitochondrial membrane density and reduced level of intracellular NADH, but not ATP (Table 1) [159,160]. Several metabolic signaling pathways and related regulators have been shown to modulate cell sensitivity to ferroptosis in different experimental settings [159,[161][162][163]. The immunomodulatory role of ferroptosis has also been investigated and discussed [164].…”

Section: An Overview Of Ferroptosismentioning

confidence: 99%

Non-Apoptotic Cell Death Signaling Pathways in Melanoma

Hartman

2020

IJMS

View full text Add to dashboard Cite

Resisting cell death is a hallmark of cancer. Disturbances in the execution of cell death programs promote carcinogenesis and survival of cancer cells under unfavorable conditions, including exposition to anti-cancer therapies. Specific modalities of regulated cell death (RCD) have been classified based on different criteria, including morphological features, biochemical alterations and immunological consequences. Although melanoma cells are broadly equipped with the anti-apoptotic machinery and recurrent genetic alterations in the components of the RAS/RAF/MEK/ERK signaling markedly contribute to the pro-survival phenotype of melanoma, the roles of autophagy-dependent cell death, necroptosis, ferroptosis, pyroptosis, and parthanatos have recently gained great interest. These signaling cascades are involved in melanoma cell response and resistance to the therapeutics used in the clinic, including inhibitors of BRAF mut and MEK1/2, and immunotherapy. In addition, the relationships between sensitivity to non-apoptotic cell death routes and specific cell phenotypes have been demonstrated, suggesting that plasticity of melanoma cells can be exploited to modulate response of these cells to different cell death stimuli. In this review, the current knowledge on the non-apoptotic cell death signaling pathways in melanoma cell biology and response to anti-cancer drugs has been discussed.

show abstract

Section: An Overview Of Ferroptosismentioning

confidence: 99%

Non-Apoptotic Cell Death Signaling Pathways in Melanoma

Hartman

2020

IJMS

View full text Add to dashboard Cite

show abstract

“…When system x c − transport cystine is blocked, the intracellular Cys levels are reduced, resulting in a decrease in GSH synthesis, a loss of GPX4 activity, intracellular lipid ROS accumulation, and ferroptosis. Inducers such as erastin can reduce intracellular Cys levels, inhibit GSH synthesis, and attenuate the accumulation of intracellular lipid ROS, leading to the development of ferroptosis by inhibiting the activity of system x c − (Dai et al, 2020 ; Wang et al, 2020 ).…”

Section: Mechanism Of Ferroptosismentioning

confidence: 99%

Insight Into the Role of Ferroptosis in Non-neoplastic Neurological Diseases

Lei

Chen

Song

et al. 2020

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Ferroptosis is an iron-dependent form of cell death characterized by the accumulation of intracellular lipid reactive oxygen species (ROS). Ferroptosis is significantly different from other types of cell death including apoptosis, autophagy, and necrosis, both in morphology and biochemical characteristics. The mechanisms that are associated with ferroptosis include iron metabolism, lipid oxidation, and other pathophysiological changes. Ferroptosis inducers or inhibitors can influence its occurrence through different pathways. Ferroptosis was initially discovered in tumors, though recent studies have confirmed that it is also closely related to a variety of neurological diseases including neurodegenerative disease [Alzheimer's disease (AD), Parkinson's disease (PD), etc.] and stroke. This article reviews the definition and characteristics of ferroptosis, the potential mechanisms associated with its development, inducers/inhibitors, and its role in non-neoplastic neurological diseases. We hope to provide a theoretical basis and novel treatment strategies for the treatment of central nervous system diseases by targeting ferroptosis.

show abstract

“…In recent years, Nrf2 antioxidant activity has been implicated in protection against ferroptosis, a recently described form of cell death caused by iron-dependent lipid peroxidation [ 34 , 35 , 36 , 37 , 38 , 39 , 40 ]. The free form of iron is indeed responsible for the Fenton reaction involving hydroxyl radical production that could propagate and trigger the accumulation of reactive lipid peroxides, the general hallmarks of ferroptosis [ 40 ].…”

Section: Introductionmentioning

confidence: 99%

“…A broad range of Nrf2-dependent genes can influence the susceptibility to ferroptosis. These genes include those involved in GSH biosynthesis and recycling, in heme and iron homeostasis, and in the NAD(P)H-producing pathway among many others [ 28 , 29 , 34 , 35 , 39 , 41 , 42 , 43 , 44 ].…”

Section: Introductionmentioning

confidence: 99%

Fasting Drives Nrf2-Related Antioxidant Response in Skeletal Muscle

Lettieri-Barbato

Minopoli

Caggiano

et al. 2020

IJMS

View full text Add to dashboard Cite

A common metabolic condition for living organisms is starvation/fasting, a state that could play systemic-beneficial roles. Complex adaptive responses are activated during fasting to help the organism to maintain energy homeostasis and avoid nutrient stress. Metabolic rearrangements during fasting cause mild oxidative stress in skeletal muscle. The nuclear factor erythroid 2-related factor 2 (Nrf2) controls adaptive responses and remains the major regulator of quenching mechanisms underlying different types of stress. Here, we demonstrate a positive role of fasting as a protective mechanism against oxidative stress in skeletal muscle. In particular, by using in vivo and in vitro models of fasting, we found that typical Nrf2-dependent genes, including those controlling iron (e.g., Ho-1) and glutathione (GSH) metabolism (e.g., Gcl, Gsr) are induced along with increased levels of the glutathione peroxidase 4 (Gpx4), a GSH-dependent antioxidant enzyme. These events are associated with a significant reduction in malondialdehyde, a well-known by-product of lipid peroxidation. Our results suggest that fasting could be a valuable approach to boost the adaptive anti-oxidant responses in skeletal muscle.

show abstract

Transcription factors in ferroptotic cell death

Cited by 171 publications

References 96 publications

Non-Apoptotic Cell Death Signaling Pathways in Melanoma

Non-Apoptotic Cell Death Signaling Pathways in Melanoma

Insight Into the Role of Ferroptosis in Non-neoplastic Neurological Diseases

Fasting Drives Nrf2-Related Antioxidant Response in Skeletal Muscle

Contact Info

Product

Resources

About