IronSulferCluV1, Main, Exploration, bibRecord, 000201

Targeting NRF2 for the Treatment of Friedreich's Ataxia: A Comparison among Drugs.

Identifieur interne : 000201 ( Main/Exploration ); précédent : 000200; suivant : 000202

Targeting NRF2 for the Treatment of Friedreich's Ataxia: A Comparison among Drugs.

Auteurs : Sara Petrillo [Italie] ; Jessica D'Amico [Italie] ; Piergiorgio La Rosa [Italie] ; Enrico Silvio Bertini [Italie] ; Fiorella Piemonte [Italie]

Source :

International journal of molecular sciences [ 1422-0067 ] ; 2019.

RBID : pubmed:31640150

Descripteurs français

KwdFr :
- Activation de la transcription (effets des médicaments et des substances chimiques), Acétylcystéine (pharmacologie), Ataxie de Friedreich (anatomopathologie), Ataxie de Friedreich (métabolisme), Ataxie de Friedreich (traitement médicamenteux), Biopsie (MeSH), Facteur-2 apparenté à NF-E2 (métabolisme), Facteurs temps (MeSH), Humains (MeSH), Isothiocyanates (pharmacologie), Oxydoréduction (MeSH), Protéines de liaison au fer (métabolisme), Régulation négative (effets des médicaments et des substances chimiques), Thérapie moléculaire ciblée (MeSH), Transduction du signal (effets des médicaments et des substances chimiques), Évaluation préclinique de médicament (MeSH).
MESH :
- anatomopathologie : Ataxie de Friedreich.
- effets des médicaments et des substances chimiques : Activation de la transcription, Régulation négative, Transduction du signal.
- métabolisme : Ataxie de Friedreich, Facteur-2 apparenté à NF-E2, Protéines de liaison au fer.
- pharmacologie : Acétylcystéine, Isothiocyanates.
- traitement médicamenteux : Ataxie de Friedreich.
- Biopsie, Facteurs temps, Humains, Oxydoréduction, Thérapie moléculaire ciblée, Évaluation préclinique de médicament.

English descriptors

KwdEn :
- Acetylcysteine (pharmacology), Biopsy (MeSH), Down-Regulation (drug effects), Drug Evaluation, Preclinical (MeSH), Friedreich Ataxia (drug therapy), Friedreich Ataxia (metabolism), Friedreich Ataxia (pathology), Humans (MeSH), Iron-Binding Proteins (metabolism), Isothiocyanates (pharmacology), Molecular Targeted Therapy (MeSH), NF-E2-Related Factor 2 (metabolism), Oxidation-Reduction (MeSH), Signal Transduction (drug effects), Time Factors (MeSH), Transcriptional Activation (drug effects).
MESH :
- chemical , metabolism : Iron-Binding Proteins, NF-E2-Related Factor 2.
- chemical , pharmacology : Acetylcysteine, Isothiocyanates.
- drug effects : Down-Regulation, Signal Transduction, Transcriptional Activation.
- drug therapy : Friedreich Ataxia.
- metabolism : Friedreich Ataxia.
- pathology : Friedreich Ataxia.
- Biopsy, Drug Evaluation, Preclinical, Humans, Molecular Targeted Therapy, Oxidation-Reduction, Time Factors.

Abstract

NRF2 (Nuclear factor Erythroid 2-related Factor 2) signaling is impaired in Friedreich's Ataxia (FRDA), an autosomal recessive disease characterized by progressive nervous system damage and degeneration of nerve fibers in the spinal cord and peripheral nerves. The loss of frataxin in patients results in iron sulfur cluster deficiency and iron accumulation in the mitochondria, making FRDA a fatal and debilitating condition. There are no currently approved therapies for the treatment of FRDA and molecules able to activate NRF2 have the potential to induce clinical benefits in patients. In this study, we compared the efficacy of six redox-active drugs, some already adopted in clinical trials, targeting NRF2 activation and frataxin expression in fibroblasts obtained from skin biopsies of FRDA patients. All of these drugs consistently increased NRF2 expression, but differential profiles of NRF2 downstream genes were activated. The Sulforaphane and N-acetylcysteine were particularly effective on genes involved in preventing inflammation and maintaining glutathione homeostasis, the dimethyl fumarate, omaxevolone, and EPI-743 in counteracting toxic products accumulation, the idebenone in mitochondrial protection. This study may contribute to develop synergic therapies, based on a combination of treatment molecules.

DOI: 10.3390/ijms20205211
PubMed: 31640150
PubMed Central: PMC6829337

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000211
to stream Main, to step Curation: 000211

Le document en format XML

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<term>Biopsy (MeSH)</term>
<term>Down-Regulation (drug effects)</term>
<term>Drug Evaluation, Preclinical (MeSH)</term>
<term>Friedreich Ataxia (drug therapy)</term>
<term>Friedreich Ataxia (metabolism)</term>
<term>Friedreich Ataxia (pathology)</term>
<term>Humans (MeSH)</term>
<term>Iron-Binding Proteins (metabolism)</term>
<term>Isothiocyanates (pharmacology)</term>
<term>Molecular Targeted Therapy (MeSH)</term>
<term>NF-E2-Related Factor 2 (metabolism)</term>
<term>Oxidation-Reduction (MeSH)</term>
<term>Signal Transduction (drug effects)</term>
<term>Time Factors (MeSH)</term>
<term>Transcriptional Activation (drug effects)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Activation de la transcription (effets des médicaments et des substances chimiques)</term>
<term>Acétylcystéine (pharmacologie)</term>
<term>Ataxie de Friedreich (anatomopathologie)</term>
<term>Ataxie de Friedreich (métabolisme)</term>
<term>Ataxie de Friedreich (traitement médicamenteux)</term>
<term>Biopsie (MeSH)</term>
<term>Facteur-2 apparenté à NF-E2 (métabolisme)</term>
<term>Facteurs temps (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Isothiocyanates (pharmacologie)</term>
<term>Oxydoréduction (MeSH)</term>
<term>Protéines de liaison au fer (métabolisme)</term>
<term>Régulation négative (effets des médicaments et des substances chimiques)</term>
<term>Thérapie moléculaire ciblée (MeSH)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
<term>Évaluation préclinique de médicament (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Iron-Binding Proteins</term>
<term>NF-E2-Related Factor 2</term>
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<term>Signal Transduction</term>
<term>Transcriptional Activation</term>
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<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Activation de la transcription</term>
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<term>Transduction du signal</term>
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<term>Protéines de liaison au fer</term>
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<term>Oxidation-Reduction</term>
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<term>Facteurs temps</term>
<term>Humains</term>
<term>Oxydoréduction</term>
<term>Thérapie moléculaire ciblée</term>
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<front><div type="abstract" xml:lang="en">NRF2 (Nuclear factor Erythroid 2-related Factor 2) signaling is impaired in Friedreich's Ataxia (FRDA), an autosomal recessive disease characterized by progressive nervous system damage and degeneration of nerve fibers in the spinal cord and peripheral nerves. The loss of frataxin in patients results in iron sulfur cluster deficiency and iron accumulation in the mitochondria, making FRDA a fatal and debilitating condition. There are no currently approved therapies for the treatment of FRDA and molecules able to activate NRF2 have the potential to induce clinical benefits in patients. In this study, we compared the efficacy of six redox-active drugs, some already adopted in clinical trials, targeting NRF2 activation and frataxin expression in fibroblasts obtained from skin biopsies of FRDA patients. All of these drugs consistently increased NRF2 expression, but differential profiles of NRF2 downstream genes were activated. The Sulforaphane and <i>N</i>
-acetylcysteine were particularly effective on genes involved in preventing inflammation and maintaining glutathione homeostasis, the dimethyl fumarate, omaxevolone, and EPI-743 in counteracting toxic products accumulation, the idebenone in mitochondrial protection. This study may contribute to develop synergic therapies, based on a combination of treatment molecules.</div>
</front>
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<DateCompleted><Year>2020</Year>
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<Abstract><AbstractText>NRF2 (Nuclear factor Erythroid 2-related Factor 2) signaling is impaired in Friedreich's Ataxia (FRDA), an autosomal recessive disease characterized by progressive nervous system damage and degeneration of nerve fibers in the spinal cord and peripheral nerves. The loss of frataxin in patients results in iron sulfur cluster deficiency and iron accumulation in the mitochondria, making FRDA a fatal and debilitating condition. There are no currently approved therapies for the treatment of FRDA and molecules able to activate NRF2 have the potential to induce clinical benefits in patients. In this study, we compared the efficacy of six redox-active drugs, some already adopted in clinical trials, targeting NRF2 activation and frataxin expression in fibroblasts obtained from skin biopsies of FRDA patients. All of these drugs consistently increased NRF2 expression, but differential profiles of NRF2 downstream genes were activated. The Sulforaphane and <i>N</i>
-acetylcysteine were particularly effective on genes involved in preventing inflammation and maintaining glutathione homeostasis, the dimethyl fumarate, omaxevolone, and EPI-743 in counteracting toxic products accumulation, the idebenone in mitochondrial protection. This study may contribute to develop synergic therapies, based on a combination of treatment molecules.</AbstractText>
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<ForeName>Jessica</ForeName>
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<AffiliationInfo><Affiliation>Unit of Muscular and Neurodegenerative Diseases, Bambino Gesù Children's Hospital, IRCCS, 00146 Rome, Italy. jessica.damico@opbg.net.</Affiliation>
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<Author ValidYN="Y"><LastName>Piemonte</LastName>
<ForeName>Fiorella</ForeName>
<Initials>F</Initials>
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<Keyword MajorTopicYN="N">Nrf2</Keyword>
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   |texte=   Targeting NRF2 for the Treatment of Friedreich's Ataxia: A Comparison among Drugs.
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Targeting NRF2 for the Treatment of Friedreich's Ataxia: A Comparison among Drugs.

Targeting NRF2 for the Treatment of Friedreich's Ataxia: A Comparison among Drugs.

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