Oxidative Damage and Antioxidant Defense in Ferroptosis

Kuang, Feimei; Liu, Jiao; Tang, Daolin; Kang, Rui

doi:10.3389/fcell.2020.586578

Cited by 297 publications

(222 citation statements)

References 120 publications

Supporting

Mentioning

197

Contrasting

Order By: Relevance

“…Our results indicated that iron overload played detrimental effects in OA progression, however, how excess iron damages chondrocytes under OA pathogenic conditions remains unknown. Excess free iron could act as a catalyst to produce large amount of ROS and lead to accumulation of lipid peroxides and ferroptosis (Kuang et al, 2020). Ferroptosis is a newly identified iron dependent cell death and we speculate that ferroptosis is involved in iron overload induced chondrocytes apoptosis.…”

Section: Figure 6 | Inhibition Of Dmt1 Restored Il-1β Induced Chondromentioning

confidence: 81%

Iron Overload Is Associated With Accelerated Progression of Osteoarthritis: The Role of DMT1 Mediated Iron Homeostasis

Jing

Lin

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Objective: Iron overload is common in elderly people which is associated with an increased prevalence of osteoarthritis (OA), but the exact role of iron in the development of OA has not been established. The aim of the present study is to elucidate the connection between iron overload and OA using an iron overloaded mice model, as well as to explore the role of iron homeostasis, iron transporters dependent iron influx in OA pathogenesis.Methods: The iron overloaded mice model was established and OA was surgically induced. OA progression was assessed at 8 weeks after surgery. Next, primary chondrocytes were treated with pro-inflammatory cytokines and iron regulators mediated iron homeostasis were evaluated. Involvement of iron transporters was analyzed using chondrocytes mimicking an osteoarthritis-related phenotype in vitro.Results: Iron overloaded mice exhibited greater cartilage destruction and elevated ADAMTS5 as well as MMP13 expression along with increased iron accumulation and dysregulated iron regulators. Pro-inflammatory cytokines could disturb cellular iron homeostasis via upregulating iron import proteins, TFR1 and DMT1, downregulating iron efflux protein FPN, thus result in cellular iron overload. Among iron transporters, DMT1 was found to play pivotal roles in iron overload induced OA progress. Inhibition of DMT1 suppressed IL-1β induced inflammatory response and ECM degradation via blockade of MAPK and PI3K/AKT/NF-κB pathways.Conclusions: Our results suggest that iron takes parts in the development of OA and cutting iron influx via inhibiting DMT1 activity could be an attractive new target for OA treatment.

show abstract

Section: Figure 6 | Inhibition Of Dmt1 Restored Il-1β Induced Chondromentioning

confidence: 81%

Iron Overload Is Associated With Accelerated Progression of Osteoarthritis: The Role of DMT1 Mediated Iron Homeostasis

Jing

Lin

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

show abstract

“… 56 GSH scavenge ROS and free radicals to protect cells from oxidative damage. 57 Main antioxidant enzymes are GPx, SOD, and CAT. GPx is mainly responsible for removal of hydroperoxides, hence, it may protect membranes, lipids, and proteins from oxidation.…”

Section: Resultsmentioning

confidence: 99%

SnO2-Doped ZnO/Reduced Graphene Oxide Nanocomposites: Synthesis, Characterization, and Improved Anticancer Activity via Oxidative Stress Pathway

Ahamed

Akhtar

Khan

et al. 2021

IJN

View full text Add to dashboard Cite

“…Excess of free reactive iron can cause various types of cell death, including a recently recognized type, ferroptosis. Although the core molecular effector of ferroptosis is unclear, ferroptosis is induced by the activation of iron-dependent lipid peroxidation ( Kuang et al, 2020 ). Significant progress has been made in dissecting the mechanisms that lead to lipid peroxidation and how antioxidant systems or stress proteins regulate ferroptosis.…”

Section: Discussionmentioning

confidence: 99%

Iron Metabolism in Ferroptosis

Chen

Kang

et al. 2020

Front. Cell Dev. Biol.

Self Cite

472

382

View full text Add to dashboard Cite

Ferroptosis is a form of regulated cell death that is characterized by iron-dependent oxidative damage and subsequent plasma membrane ruptures and the release of damage-associated molecular patterns. Due to the role of iron in mediating the production of reactive oxygen species and enzyme activity in lipid peroxidation, ferroptosis is strictly controlled by regulators involved in many aspects of iron metabolism, such as iron uptake, storage, utilization, and efflux. Translational and transcriptional regulation of iron homeostasis provide an integrated network to determine the sensitivity of ferroptosis. Impaired ferroptosis is implicated in various iron-related pathological conditions or diseases, such as cancer, neurodegenerative diseases, and ischemia-reperfusion injury. Understanding the molecular mechanisms underlying the regulation of iron metabolism during ferroptosis may provide effective strategies for the treatment of ferroptosis-associated diseases. Indeed, iron chelators effectively prevent the occurrence of ferroptosis, which may provide new approaches for the treatment of iron-related disorders. In this review, we summarize recent advances in the theoretical modeling of iron-dependent ferroptosis, and highlight the therapeutic implications of iron chelators in diseases.

show abstract

Oxidative Damage and Antioxidant Defense in Ferroptosis

Cited by 297 publications

References 120 publications

Iron Overload Is Associated With Accelerated Progression of Osteoarthritis: The Role of DMT1 Mediated Iron Homeostasis

Iron Overload Is Associated With Accelerated Progression of Osteoarthritis: The Role of DMT1 Mediated Iron Homeostasis

SnO2-Doped ZnO/Reduced Graphene Oxide Nanocomposites: Synthesis, Characterization, and Improved Anticancer Activity via Oxidative Stress Pathway

Iron Metabolism in Ferroptosis

Contact Info

Product

Resources

About