Ferroptosis in Friedreich's Ataxia: A Metal-Induced Neurodegenerative Disease.
Identifieur interne : 000123 ( Main/Exploration ); précédent : 000122; suivant : 000124Ferroptosis in Friedreich's Ataxia: A Metal-Induced Neurodegenerative Disease.
Auteurs : Piergiorgio La Rosa [Italie] ; Sara Petrillo [Italie] ; Maria Teresa Fiorenza [Italie] ; Enrico Silvio Bertini [Italie] ; Fiorella Piemonte [Italie]Source :
- Biomolecules [ 2218-273X ] ; 2020.
Abstract
Ferroptosis is an iron-dependent form of regulated cell death, arising from the accumulation of lipid-based reactive oxygen species when glutathione-dependent repair systems are compromised. Lipid peroxidation, mitochondrial impairment and iron dyshomeostasis are the hallmark of ferroptosis, which is emerging as a crucial player in neurodegeneration. This review provides an analysis of the most recent advances in ferroptosis, with a special focus on Friedreich's Ataxia (FA), the most common autosomal recessive neurodegenerative disease, caused by reduced levels of frataxin, a mitochondrial protein involved in iron-sulfur cluster synthesis and antioxidant defenses. The hypothesis is that the iron-induced oxidative damage accumulates over time in FA, lowering the ferroptosis threshold and leading to neuronal cell death and, at last, to cardiac failure. The use of anti-ferroptosis drugs combined with treatments able to activate the antioxidant response will be of paramount importance in FA therapy, such as in many other neurodegenerative diseases triggered by oxidative stress.
DOI: 10.3390/biom10111551
PubMed: 33202971
Affiliations:
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Neurodegenerative Diseases, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Unit of Muscular and Neurodegenerative Diseases, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome</wicri:regionArea><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author><author><name sortKey="Piemonte, Fiorella" sort="Piemonte, Fiorella" uniqKey="Piemonte F" first="Fiorella" last="Piemonte">Fiorella Piemonte</name><affiliation wicri:level="1"><nlm:affiliation>Unit of Muscular and Neurodegenerative Diseases, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Unit of Muscular and Neurodegenerative Diseases, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome</wicri:regionArea><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author></analytic><series><title level="j">Biomolecules</title><idno type="eISSN">2218-273X</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Ferroptosis is an iron-dependent form of regulated cell death, arising from the accumulation of lipid-based reactive oxygen species when glutathione-dependent repair systems are compromised. Lipid peroxidation, mitochondrial impairment and iron dyshomeostasis are the hallmark of ferroptosis, which is emerging as a crucial player in neurodegeneration. This review provides an analysis of the most recent advances in ferroptosis, with a special focus on Friedreich's Ataxia (FA), the most common autosomal recessive neurodegenerative disease, caused by reduced levels of frataxin, a mitochondrial protein involved in iron-sulfur cluster synthesis and antioxidant defenses. The hypothesis is that the iron-induced oxidative damage accumulates over time in FA, lowering the ferroptosis threshold and leading to neuronal cell death and, at last, to cardiac failure. The use of anti-ferroptosis drugs combined with treatments able to activate the antioxidant response will be of paramount importance in FA therapy, such as in many other neurodegenerative diseases triggered by oxidative stress.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">33202971</PMID><DateRevised><Year>2020</Year><Month>11</Month><Day>18</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2218-273X</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>11</Issue><PubDate><Year>2020</Year><Month>Nov</Month><Day>13</Day></PubDate></JournalIssue><Title>Biomolecules</Title><ISOAbbreviation>Biomolecules</ISOAbbreviation></Journal><ArticleTitle>Ferroptosis in Friedreich's Ataxia: A Metal-Induced Neurodegenerative Disease.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">E1551</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/biom10111551</ELocationID><Abstract><AbstractText>Ferroptosis is an iron-dependent form of regulated cell death, arising from the accumulation of lipid-based reactive oxygen species when glutathione-dependent repair systems are compromised. Lipid peroxidation, mitochondrial impairment and iron dyshomeostasis are the hallmark of ferroptosis, which is emerging as a crucial player in neurodegeneration. This review provides an analysis of the most recent advances in ferroptosis, with a special focus on Friedreich's Ataxia (FA), the most common autosomal recessive neurodegenerative disease, caused by reduced levels of frataxin, a mitochondrial protein involved in iron-sulfur cluster synthesis and antioxidant defenses. The hypothesis is that the iron-induced oxidative damage accumulates over time in FA, lowering the ferroptosis threshold and leading to neuronal cell death and, at last, to cardiac failure. The use of anti-ferroptosis drugs combined with treatments able to activate the antioxidant response will be of paramount importance in FA therapy, such as in many other neurodegenerative diseases triggered by oxidative stress.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>La Rosa</LastName><ForeName>Piergiorgio</ForeName><Initials>P</Initials><Identifier Source="ORCID">0000-0002-9723-2363</Identifier><AffiliationInfo><Affiliation>Department of Psychology, Division of Neuroscience, Sapienza University of Rome, 00185 Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Petrillo</LastName><ForeName>Sara</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Unit of Muscular and Neurodegenerative Diseases, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fiorenza</LastName><ForeName>Maria Teresa</ForeName><Initials>MT</Initials><Identifier Source="ORCID">0000-0002-5079-4019</Identifier><AffiliationInfo><Affiliation>Department of Psychology, Division of Neuroscience, Sapienza University of Rome, 00185 Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bertini</LastName><ForeName>Enrico Silvio</ForeName><Initials>ES</Initials><Identifier Source="ORCID">0000-0001-9276-4590</Identifier><AffiliationInfo><Affiliation>Unit of Muscular and Neurodegenerative Diseases, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Piemonte</LastName><ForeName>Fiorella</ForeName><Initials>F</Initials><Identifier Source="ORCID">0000-0003-1825-9347</Identifier><AffiliationInfo><Affiliation>Unit of Muscular and Neurodegenerative Diseases, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>11</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Biomolecules</MedlineTA><NlmUniqueID>101596414</NlmUniqueID><ISSNLinking>2218-273X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Friedreich’s Ataxia</Keyword><Keyword MajorTopicYN="N">ferroptosis</Keyword><Keyword MajorTopicYN="N">iron</Keyword><Keyword MajorTopicYN="N">neurodegeneration</Keyword><Keyword MajorTopicYN="N">oxidative stress</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>09</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>11</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>11</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>11</Month><Day>18</Day><Hour>1</Hour><Minute>2</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>11</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>11</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">33202971</ArticleId><ArticleId IdType="pii">biom10111551</ArticleId><ArticleId IdType="doi">10.3390/biom10111551</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Italie</li></country><region><li>Latium</li></region><settlement><li>Rome</li></settlement></list><tree><country name="Italie"><region name="Latium"><name sortKey="La Rosa, Piergiorgio" sort="La Rosa, Piergiorgio" uniqKey="La Rosa P" first="Piergiorgio" last="La Rosa">Piergiorgio La Rosa</name></region><name sortKey="Bertini, Enrico Silvio" sort="Bertini, Enrico Silvio" uniqKey="Bertini E" first="Enrico Silvio" last="Bertini">Enrico Silvio Bertini</name><name sortKey="Fiorenza, Maria Teresa" sort="Fiorenza, Maria Teresa" uniqKey="Fiorenza M" first="Maria Teresa" last="Fiorenza">Maria Teresa Fiorenza</name><name sortKey="Petrillo, Sara" sort="Petrillo, Sara" uniqKey="Petrillo S" first="Sara" last="Petrillo">Sara Petrillo</name><name sortKey="Piemonte, Fiorella" sort="Piemonte, Fiorella" uniqKey="Piemonte F" first="Fiorella" last="Piemonte">Fiorella Piemonte</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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