Metabolic Targets for Treatment of Autoimmune Diseases.
Identifieur interne : 000088 ( Main/Exploration ); précédent : 000087; suivant : 000089Metabolic Targets for Treatment of Autoimmune Diseases.
Auteurs : Paramarjan Piranavan [États-Unis] ; Manjeet Bhamra [États-Unis] ; Andras Perl [États-Unis]Source :
- Immunometabolism [ 2084-6835 ] ; 2020.
Abstract
There is a considerable unmet demand for safe and efficacious medications in the realm of autoimmune and inflammatory diseases. The fate of the immune cells is precisely governed by control of various metabolic processes such as mitochondrial oxidative phosphorylation, glycolysis, fatty acid synthesis, beta-oxidation, amino acid metabolism, and several others including the pentose phosphate pathway, which is a unique source of metabolites for cell proliferation and maintenance of a reducing environment. These pathways are tightly regulated by the cytokines, growth factors, availability of the nutrients and host-microbe interaction. Exploring the immunometabolic pathways that govern the fate of cells of the innate and adaptive immune system, during various stages of activation, proliferation, differentiation and effector response, is crucial for new development of new treatment targets. Identifying the pathway connections and key enzymes will help us to target the dysregulated inflammation in autoimmune diseases. The mechanistic target of rapamycin (mTOR) pathway is increasingly recognized as one of the key drivers of proinflammatory responses in autoimmune diseases. In this review, we provide an update on the current understanding of the metabolic signatures noted within different immune cells of many different autoimmune diseases with a focus on selecting pathways and specific metabolites as targets for treatment.
DOI: 10.20900/immunometab20200012
PubMed: 32341806
PubMed Central: PMC7184931
Affiliations:
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University of New York, Syracuse, NY 13210</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Bhamra, Manjeet" sort="Bhamra, Manjeet" uniqKey="Bhamra M" first="Manjeet" last="Bhamra">Manjeet Bhamra</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, College of Medicine, State University of New York, Syracuse, NY 13210, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, College of Medicine, State University of New York, Syracuse, NY 13210</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Perl, Andras" sort="Perl, Andras" uniqKey="Perl A" first="Andras" last="Perl">Andras Perl</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, College of Medicine, State University of New York, Syracuse, NY 13210, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, College of Medicine, State University of New York, Syracuse, NY 13210</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, College of Medicine, State University of New York, Syracuse, NY 13210, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, College of Medicine, State University of New York, Syracuse, NY 13210</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation><affiliation wicri:level="2"><nlm:affiliation>Department of Biochemistry and Molecular Biology, College of Medicine, State University of New York, Syracuse, NY 13210, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biochemistry and Molecular Biology, College of Medicine, State University of New York, Syracuse, NY 13210</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author></analytic><series><title level="j">Immunometabolism</title><idno type="ISSN">2084-6835</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">There is a considerable unmet demand for safe and efficacious medications in the realm of autoimmune and inflammatory diseases. The fate of the immune cells is precisely governed by control of various metabolic processes such as mitochondrial oxidative phosphorylation, glycolysis, fatty acid synthesis, beta-oxidation, amino acid metabolism, and several others including the pentose phosphate pathway, which is a unique source of metabolites for cell proliferation and maintenance of a reducing environment. These pathways are tightly regulated by the cytokines, growth factors, availability of the nutrients and host-microbe interaction. Exploring the immunometabolic pathways that govern the fate of cells of the innate and adaptive immune system, during various stages of activation, proliferation, differentiation and effector response, is crucial for new development of new treatment targets. Identifying the pathway connections and key enzymes will help us to target the dysregulated inflammation in autoimmune diseases. The mechanistic target of rapamycin (mTOR) pathway is increasingly recognized as one of the key drivers of proinflammatory responses in autoimmune diseases. In this review, we provide an update on the current understanding of the metabolic signatures noted within different immune cells of many different autoimmune diseases with a focus on selecting pathways and specific metabolites as targets for treatment.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">32341806</PMID><DateRevised><Year>2020</Year><Month>09</Month><Day>28</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">2084-6835</ISSN><JournalIssue CitedMedium="Print"><Volume>2</Volume><Issue>2</Issue><PubDate><Year>2020</Year></PubDate></JournalIssue><Title>Immunometabolism</Title><ISOAbbreviation>Immunometabolism</ISOAbbreviation></Journal><ArticleTitle>Metabolic Targets for Treatment of Autoimmune Diseases.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">e200012</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.20900/immunometab20200012</ELocationID><Abstract><AbstractText>There is a considerable unmet demand for safe and efficacious medications in the realm of autoimmune and inflammatory diseases. The fate of the immune cells is precisely governed by control of various metabolic processes such as mitochondrial oxidative phosphorylation, glycolysis, fatty acid synthesis, beta-oxidation, amino acid metabolism, and several others including the pentose phosphate pathway, which is a unique source of metabolites for cell proliferation and maintenance of a reducing environment. These pathways are tightly regulated by the cytokines, growth factors, availability of the nutrients and host-microbe interaction. Exploring the immunometabolic pathways that govern the fate of cells of the innate and adaptive immune system, during various stages of activation, proliferation, differentiation and effector response, is crucial for new development of new treatment targets. Identifying the pathway connections and key enzymes will help us to target the dysregulated inflammation in autoimmune diseases. The mechanistic target of rapamycin (mTOR) pathway is increasingly recognized as one of the key drivers of proinflammatory responses in autoimmune diseases. In this review, we provide an update on the current understanding of the metabolic signatures noted within different immune cells of many different autoimmune diseases with a focus on selecting pathways and specific metabolites as targets for treatment.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Piranavan</LastName><ForeName>Paramarjan</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Medicine, College of Medicine, State University of New York, Syracuse, NY 13210, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bhamra</LastName><ForeName>Manjeet</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medicine, College of Medicine, State University of New York, Syracuse, NY 13210, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Perl</LastName><ForeName>Andras</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Medicine, College of Medicine, State University of New York, Syracuse, NY 13210, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, College of Medicine, State University of New York, Syracuse, NY 13210, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, College of Medicine, State University of New York, Syracuse, NY 13210, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AI072648</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI122176</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R34 AI141304</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R34 AR068052</GrantID><Acronym>AR</Acronym><Agency>NIAMS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>03</Month><Day>31</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Immunometabolism</MedlineTA><NlmUniqueID>101607751</NlmUniqueID></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">acetylcysteine</Keyword><Keyword MajorTopicYN="N">glycolysis</Keyword><Keyword MajorTopicYN="N">immune metabolic pathways</Keyword><Keyword MajorTopicYN="N">kynurenine</Keyword><Keyword MajorTopicYN="N">mechanistic target of rapamycin</Keyword><Keyword MajorTopicYN="N">oxidative phosphorylation</Keyword><Keyword MajorTopicYN="N">oxidative stress</Keyword><Keyword MajorTopicYN="N">pentose phosphate pathway</Keyword><Keyword MajorTopicYN="N">psoriasis</Keyword><Keyword MajorTopicYN="N">rheumatoid arthritis</Keyword><Keyword MajorTopicYN="N">scleroderma</Keyword><Keyword MajorTopicYN="N">systemic lupus erythematosus</Keyword><Keyword MajorTopicYN="N">tryptophan</Keyword></KeywordList><CoiStatement>CONFLICTS OF INTEREST The authors declare that they have no conflicts of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>4</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>4</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>4</Month><Day>29</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32341806</ArticleId><ArticleId IdType="doi">10.20900/immunometab20200012</ArticleId><ArticleId IdType="pmc">PMC7184931</ArticleId><ArticleId IdType="mid">NIHMS1580994</ArticleId></ArticleIdList><pmc-dir>nihms</pmc-dir>
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