Metabolic pathways mediate pathogenesis and offer targets for treatment in rheumatic diseases.
Identifieur interne : 000086 ( Main/Exploration ); précédent : 000085; suivant : 000087Metabolic pathways mediate pathogenesis and offer targets for treatment in rheumatic diseases.
Auteurs : Brandon Wyman [États-Unis] ; Andras Perl [États-Unis]Source :
- Current opinion in rheumatology [ 1531-6963 ] ; 2020.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cellules endothéliales (métabolisme), Différenciation cellulaire (MeSH), Humains (MeSH), Inflammation (métabolisme), Lymphocytes T régulateurs (métabolisme), Maladies auto-immunes (métabolisme), Maladies auto-immunes (traitement médicamenteux), Rhumatismes (métabolisme), Rhumatismes (traitement médicamenteux), Sirolimus (usage thérapeutique), Souris (MeSH), Voies et réseaux métaboliques (physiologie).
- MESH :
- métabolisme : Cellules endothéliales, Inflammation, Lymphocytes T régulateurs, Maladies auto-immunes, Rhumatismes.
- physiologie : Voies et réseaux métaboliques.
- traitement médicamenteux : Maladies auto-immunes, Rhumatismes.
- usage thérapeutique : Sirolimus.
- Animaux, Différenciation cellulaire, Humains, Souris.
English descriptors
- KwdEn :
- Animals (MeSH), Autoimmune Diseases (drug therapy), Autoimmune Diseases (metabolism), Cell Differentiation (MeSH), Endothelial Cells (metabolism), Humans (MeSH), Inflammation (metabolism), Metabolic Networks and Pathways (physiology), Mice (MeSH), Rheumatic Diseases (drug therapy), Rheumatic Diseases (metabolism), Sirolimus (therapeutic use), T-Lymphocytes, Regulatory (metabolism).
- MESH :
- chemical , therapeutic use : Sirolimus.
- drug therapy : Autoimmune Diseases, Rheumatic Diseases.
- metabolism : Autoimmune Diseases, Endothelial Cells, Inflammation, Rheumatic Diseases, T-Lymphocytes, Regulatory.
- physiology : Metabolic Networks and Pathways.
- Animals, Cell Differentiation, Humans, Mice.
Abstract
PURPOSE OF REVIEW
The cause of autoimmune diseases remains incompletely understood. Here, we highlight recent advances in the role of proinflammatory metabolic pathways in autoimmune disease, including treatment with antioxidants and mechanistic target of rapamycin (mTOR) inhibitors.
RECENT FINDINGS
Recent studies show that mTOR pathway activation, glucose utilization, mitochondrial oxidative phosphorylation, and antioxidant defenses play critical roles in the pathogenesis of autoimmune diseases, including rheumatoid arthritis, immune thrombocytopenia, Sjögren's syndrome, large vessel vasculitis, and systemic lupus erythematosus. mTOR activity leads to Th1 and Th17 cell proliferation, Treg depletion, plasma cell differentiation, macrophage dysfunction, and increased antibody and immune complex production, ultimately resulting in tissue inflammation. mTOR also affects the function of connective tissue cells, including fibroblast-like synoviocytes, endothelial cells, and podocytes. mTOR inhibition via rapamycin and N-acetylcysteine, and blockade of glucose utilization show clinical efficacy in both mouse models and clinical trials, such as systemic lupus erythematosus.
SUMMARY
The mTOR pathway is a central regulator of growth and survival signals, integrating environmental cues to control cell proliferation and differentiation. Activation of mTOR underlies inflammatory lineage specification, and mTOR blockade-based therapies show promising efficacy in several autoimmune diseases.
DOI: 10.1097/BOR.0000000000000687
PubMed: 31895126
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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York</region></placeName></affiliation></author><author><name sortKey="Perl, Andras" sort="Perl, Andras" uniqKey="Perl A" first="Andras" last="Perl">Andras Perl</name><affiliation><nlm:affiliation>Division of Rheumatology, Department of Medicine.</nlm:affiliation><wicri:noCountry code="subField">Department of Medicine</wicri:noCountry></affiliation><affiliation><nlm:affiliation>Department of Microbiology and Immunology.</nlm:affiliation><wicri:noCountry code="no comma">Department of Microbiology and Immunology.</wicri:noCountry></affiliation><affiliation wicri:level="2"><nlm:affiliation>Department of Biochemistry and Molecular Biology, State University of New York, Upstate Medical University, College of Medicine, Syracuse, New York, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, State University of New York, Upstate Medical University, College of Medicine, Syracuse, New 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(métabolisme)</term><term>Maladies auto-immunes (traitement médicamenteux)</term><term>Rhumatismes (métabolisme)</term><term>Rhumatismes (traitement médicamenteux)</term><term>Sirolimus (usage thérapeutique)</term><term>Souris (MeSH)</term><term>Voies et réseaux métaboliques (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Sirolimus</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Autoimmune Diseases</term><term>Rheumatic Diseases</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Autoimmune Diseases</term><term>Endothelial Cells</term><term>Inflammation</term><term>Rheumatic Diseases</term><term>T-Lymphocytes, Regulatory</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules endothéliales</term><term>Inflammation</term><term>Lymphocytes T régulateurs</term><term>Maladies auto-immunes</term><term>Rhumatismes</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Voies et réseaux métaboliques</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Metabolic Networks and Pathways</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Maladies auto-immunes</term><term>Rhumatismes</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Sirolimus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Differentiation</term><term>Humans</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Différenciation cellulaire</term><term>Humains</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>PURPOSE OF REVIEW</b></p><p>The cause of autoimmune diseases remains incompletely understood. Here, we highlight recent advances in the role of proinflammatory metabolic pathways in autoimmune disease, including treatment with antioxidants and mechanistic target of rapamycin (mTOR) inhibitors.</p></div><div type="abstract" xml:lang="en"><p><b>RECENT FINDINGS</b></p><p>Recent studies show that mTOR pathway activation, glucose utilization, mitochondrial oxidative phosphorylation, and antioxidant defenses play critical roles in the pathogenesis of autoimmune diseases, including rheumatoid arthritis, immune thrombocytopenia, Sjögren's syndrome, large vessel vasculitis, and systemic lupus erythematosus. mTOR activity leads to Th1 and Th17 cell proliferation, Treg depletion, plasma cell differentiation, macrophage dysfunction, and increased antibody and immune complex production, ultimately resulting in tissue inflammation. mTOR also affects the function of connective tissue cells, including fibroblast-like synoviocytes, endothelial cells, and podocytes. mTOR inhibition via rapamycin and N-acetylcysteine, and blockade of glucose utilization show clinical efficacy in both mouse models and clinical trials, such as systemic lupus erythematosus.</p></div><div type="abstract" xml:lang="en"><p><b>SUMMARY</b></p><p>The mTOR pathway is a central regulator of growth and survival signals, integrating environmental cues to control cell proliferation and differentiation. Activation of mTOR underlies inflammatory lineage specification, and mTOR blockade-based therapies show promising efficacy in several autoimmune diseases.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Curated" Owner="NLM"><PMID Version="1">31895126</PMID><DateCompleted><Year>2020</Year><Month>09</Month><Day>09</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-6963</ISSN><JournalIssue CitedMedium="Internet"><Volume>32</Volume><Issue>2</Issue><PubDate><Year>2020</Year><Month>03</Month></PubDate></JournalIssue><Title>Current opinion in rheumatology</Title><ISOAbbreviation>Curr Opin Rheumatol</ISOAbbreviation></Journal><ArticleTitle>Metabolic pathways mediate pathogenesis and offer targets for treatment in rheumatic diseases.</ArticleTitle><Pagination><MedlinePgn>184-191</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1097/BOR.0000000000000687</ELocationID><Abstract><AbstractText Label="PURPOSE OF REVIEW">The cause of autoimmune diseases remains incompletely understood. 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MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>1</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>9</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>1</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31895126</ArticleId><ArticleId IdType="doi">10.1097/BOR.0000000000000687</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Wyman, Brandon" sort="Wyman, Brandon" uniqKey="Wyman B" first="Brandon" last="Wyman">Brandon Wyman</name></region><name sortKey="Perl, Andras" sort="Perl, Andras" uniqKey="Perl A" first="Andras" last="Perl">Andras Perl</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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