Mini-Review: Is iron-mediated cell death (ferroptosis) an identical factor contributing to the pathogenesis of some neurodegenerative diseases?

Viktorínová, Alena; Ďurfinová, Monika

doi:10.1016/j.neulet.2021.135627

Cited by 25 publications

(19 citation statements)

References 61 publications

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“…Notably, the most common neurodegenerative diseases, Alzheimer's disease (AD) and Parkinson's disease (PD), are marked by deposits of insoluble protein aggregates of β-amyloids and α-synuclein, respectively, that colocalize in the brain with iron. Iron dyshomeostasis represents an early and crucial step in neurodegeneration accompanied by an altered distribution and accumulation of iron in different compartments and cell types of the brain [70][71][72]. Indeed, iron accumulation affects a cascade of intracellular processes such as iron-induced oxidative stress and lipid peroxidation that are markers of ferroptosis [73], and is also implicated in neuroinflammation by mediating proinflammatory cytokine release in glial cells [70][71][72].…”

Section: Iron Dyshomeostasis In Neurodegenerationmentioning

confidence: 99%

“…Iron dyshomeostasis represents an early and crucial step in neurodegeneration accompanied by an altered distribution and accumulation of iron in different compartments and cell types of the brain [70][71][72]. Indeed, iron accumulation affects a cascade of intracellular processes such as iron-induced oxidative stress and lipid peroxidation that are markers of ferroptosis [73], and is also implicated in neuroinflammation by mediating proinflammatory cytokine release in glial cells [70][71][72]. For example, a recent genome-wide CRISPR-based screen revealed that neuronal ROS and lipid peroxidation levels under chronic oxidative stress are modulated by mTOR, autophagy, and regulators of ferroptosis, and genes with other lysosomal functions are also implicated [53].…”

Section: Iron Dyshomeostasis In Neurodegenerationmentioning

confidence: 99%

“…In conclusion, iron contributes to key features of neurodegeneration and intersects with lysosomal pathways, whereas targeting iron dysregulationfor instance by iron chelation or possibly by blocking ferroptosismay be of therapeutic interest [70][71][72].…”

Section: Iron Dyshomeostasis In Neurodegenerationmentioning

confidence: 99%

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The lysosome as a master regulator of iron metabolism

Rizzollo

Vangheluwe

et al. 2021

Trends in Biochemical Sciences

117

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Section: Iron Dyshomeostasis In Neurodegenerationmentioning

confidence: 99%

Section: Iron Dyshomeostasis In Neurodegenerationmentioning

confidence: 99%

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The lysosome as a master regulator of iron metabolism

Rizzollo

Vangheluwe

et al. 2021

Trends in Biochemical Sciences

117

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“…The activation of the oxidative stress pathways coupled with mitochondrial dysfunction and innate immunity further exacerbate proinflammatory responses and thus play a major role in COVID-19 pathogenesis and severity [ 213 , 214 , 215 ]. Mitochondrial dysfunction and hallmark features of ferroptosis (including iron deposition, GSH depletion, and elevated lipid peroxidation, i.e., oxidative stress) are consistently observed in neurodegenerative diseases, including AD and PD [ 216 , 217 , 218 ].…”

Section: Covid-19 and Neurodegenerationmentioning

confidence: 99%

A Peek into Pandora’s Box: COVID-19 and Neurodegeneration

Chandra¹,

Johri²

2022

Brain Sciences

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Ever since it was first reported in Wuhan, China, the coronavirus-induced disease of 2019 (COVID-19) has become an enigma of sorts with ever expanding reports of direct and indirect effects of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on almost all the vital organ systems. Along with inciting acute pulmonary complications, the virus attacks the cardiac, renal, hepatic, and gastrointestinal systems as well as the central nervous system (CNS). The person-to-person variability in susceptibility of individuals to disease severity still remains a puzzle, although the comorbidities and the age/gender of a person are believed to play a key role. SARS-CoV-2 needs angiotensin-converting enzyme 2 (ACE2) receptor for its infectivity, and the association between SARS-CoV-2 and ACE2 leads to a decline in ACE2 activity and its neuroprotective effects. Acute respiratory distress may also induce hypoxia, leading to increased oxidative stress and neurodegeneration. Infection of the neurons along with peripheral leukocytes’ activation results in proinflammatory cytokine release, rendering the brain more susceptible to neurodegenerative changes. Due to the advancement in molecular biology techniques and vaccine development programs, the world now has hope to relatively quickly study and combat the deadly virus. On the other side, however, the virus seems to be still evolving with new variants being discovered periodically. In keeping up with the pace of this virus, there has been an avalanche of studies. This review provides an update on the recent progress in adjudicating the CNS-related mechanisms of SARS-CoV-2 infection and its potential to incite or accelerate neurodegeneration in surviving patients. Current as well as emerging therapeutic opportunities and biomarker development are highlighted.

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“…Iron overload, GSH exhaustion, GPX4 inactivation, and lipid peroxidation are the major features of ferroptosis. Dysregulated ferroptosis has been evidenced to be implicated in the pathogenesis and progression of many human diseases [ 196 ]. Furthermore, targeting induction of ferroptosis provides a potential therapeutic strategy for the clinical intervention of cancers, especially the other traditional therapy-resistant cancers [ 197 , 198 ].…”

Section: Conclusive Remarks and Perspectivementioning

confidence: 99%

Emerging Pathological Engagement of Ferroptosis in Gut Diseases

Gao

Zhang

2021

Oxidative Medicine and Cellular Longevity

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Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn’s disease, is mainly characterized by chronic and progressive inflammation that damages the gastrointestinal mucosa. Increasing studies have enlightened that dysregulated cell death occurs in the inflamed sites, leading to the disruption of the intestinal barrier and aggravating inflammatory response. Ferroptosis, a newly characterized form of regulated cell death, is driven by the lethal accumulation of lipid peroxides catalyzed by cellular free iron. It has been widely documented that the fundamental features of ferroptosis, including iron deposition, GSH exhaustion, GPX4 inactivation, and lipid peroxidation, are manifested in the injured gastrointestinal tract in IBD patients. Furthermore, manipulation of the critical ferroptotic genes could alter the progression, severity, or even morbidity of the experimental colitis. Herein, we critically summarize the recent advances in the field of ferroptosis, focusing on interpreting the potential engagement of ferroptosis in the pathogenesis of IBD. Moreover, we are attempting to shed light on a perspective insight into the possibility of targeting ferroptosis as novel therapeutic designs for the clinical intervention of these gastrointestinal diseases.

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Mini-Review: Is iron-mediated cell death (ferroptosis) an identical factor contributing to the pathogenesis of some neurodegenerative diseases?

Cited by 25 publications

References 61 publications

The lysosome as a master regulator of iron metabolism

The lysosome as a master regulator of iron metabolism

A Peek into Pandora’s Box: COVID-19 and Neurodegeneration

Emerging Pathological Engagement of Ferroptosis in Gut Diseases

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