Mechanisms and therapeutic significance of autophagy modulation by antipsychotic drugs.
Identifieur interne : 000555 ( Main/Exploration ); précédent : 000554; suivant : 000556Mechanisms and therapeutic significance of autophagy modulation by antipsychotic drugs.
Auteurs : Ljubica Vucicevic [Serbie] ; Maja Misirkic-Marjanovic [Serbie] ; Ljubica Harhaji-Trajkovic [Serbie] ; Nadja Maric [Serbie] ; Vladimir Trajkovic [Serbie]Source :
- Cell stress [ 2523-0204 ] ; 2018.
Abstract
In this review we analyze the ability of antipsychotic medications to modulate macroautophagy, a process of controlled lysosomal digestion of cellular macromolecules and organelles. We focus on its molecular mechanisms, consequences for the function/survival of neuronal and other cells, and the contribution to the beneficial and side-effects of antipsychotics in the treatment of schizophrenia, neurodegeneration, and cancer. A wide range of antipsychotics was able to induce neuronal autophagy as a part of the adaptive stress response apparently independent of mammalian target of rapamycin and dopamine receptor blockade. Autophagy induction by antipsychotics could contribute to reducing neuronal dysfunction in schizophrenia, but also to the adverse effects associated with their long-term use, such as brain volume loss and weight gain. In neurodegenerative diseases, antipsychotic-stimulated autophagy might help to increase the clearance and reduce neurotoxicity of aggregated proteotoxins. However, the possibility that some antipsychotics might block autophagic flux and potentially contribute to proteotoxin-mediated neurodegeneration must be considered. Finally, the anticancer effects of autophagy induction by antipsychotics make plausible their repurposing as adjuncts to standard cancer therapy.
DOI: 10.15698/cst2018.11.161
PubMed: 31225453
PubMed Central: PMC6551804
Affiliations:
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University of Belgrade, Belgrade, Serbia.</nlm:affiliation><country xml:lang="fr">Serbie</country><wicri:regionArea>Institute for Biological Research, University of Belgrade, Belgrade</wicri:regionArea><wicri:noRegion>Belgrade</wicri:noRegion></affiliation></author><author><name sortKey="Maric, Nadja" sort="Maric, Nadja" uniqKey="Maric N" first="Nadja" last="Maric">Nadja Maric</name><affiliation wicri:level="1"><nlm:affiliation>Clinic of Psychiatry, Clinical Centre of Serbia and School of Medicine, University of Belgrade, Belgrade, Serbia.</nlm:affiliation><country xml:lang="fr">Serbie</country><wicri:regionArea>Clinic of Psychiatry, Clinical Centre of Serbia and School of Medicine, University of Belgrade, Belgrade</wicri:regionArea><wicri:noRegion>Belgrade</wicri:noRegion></affiliation></author><author><name sortKey="Trajkovic, Vladimir" sort="Trajkovic, Vladimir" uniqKey="Trajkovic V" first="Vladimir" last="Trajkovic">Vladimir Trajkovic</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Microbiology and Immunology, School of Medicine, University of Belgrade, Dr. Subotica 1, 11000 Belgrade, Serbia.</nlm:affiliation><country xml:lang="fr">Serbie</country><wicri:regionArea>Institute of Microbiology and Immunology, School of Medicine, University of Belgrade, Dr. Subotica 1, 11000 Belgrade</wicri:regionArea><wicri:noRegion>11000 Belgrade</wicri:noRegion></affiliation></author></analytic><series><title level="j">Cell stress</title><idno type="eISSN">2523-0204</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In this review we analyze the ability of antipsychotic medications to modulate macroautophagy, a process of controlled lysosomal digestion of cellular macromolecules and organelles. We focus on its molecular mechanisms, consequences for the function/survival of neuronal and other cells, and the contribution to the beneficial and side-effects of antipsychotics in the treatment of schizophrenia, neurodegeneration, and cancer. A wide range of antipsychotics was able to induce neuronal autophagy as a part of the adaptive stress response apparently independent of mammalian target of rapamycin and dopamine receptor blockade. Autophagy induction by antipsychotics could contribute to reducing neuronal dysfunction in schizophrenia, but also to the adverse effects associated with their long-term use, such as brain volume loss and weight gain. In neurodegenerative diseases, antipsychotic-stimulated autophagy might help to increase the clearance and reduce neurotoxicity of aggregated proteotoxins. However, the possibility that some antipsychotics might block autophagic flux and potentially contribute to proteotoxin-mediated neurodegeneration must be considered. Finally, the anticancer effects of autophagy induction by antipsychotics make plausible their repurposing as adjuncts to standard cancer therapy.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">31225453</PMID><DateRevised><Year>2020</Year><Month>10</Month><Day>01</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2523-0204</ISSN><JournalIssue CitedMedium="Internet"><Volume>2</Volume><Issue>11</Issue><PubDate><Year>2018</Year><Month>Oct</Month><Day>25</Day></PubDate></JournalIssue><Title>Cell stress</Title><ISOAbbreviation>Cell Stress</ISOAbbreviation></Journal><ArticleTitle>Mechanisms and therapeutic significance of autophagy modulation by antipsychotic drugs.</ArticleTitle><Pagination><MedlinePgn>282-291</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.15698/cst2018.11.161</ELocationID><Abstract><AbstractText>In this review we analyze the ability of antipsychotic medications to modulate macroautophagy, a process of controlled lysosomal digestion of cellular macromolecules and organelles. We focus on its molecular mechanisms, consequences for the function/survival of neuronal and other cells, and the contribution to the beneficial and side-effects of antipsychotics in the treatment of schizophrenia, neurodegeneration, and cancer. A wide range of antipsychotics was able to induce neuronal autophagy as a part of the adaptive stress response apparently independent of mammalian target of rapamycin and dopamine receptor blockade. Autophagy induction by antipsychotics could contribute to reducing neuronal dysfunction in schizophrenia, but also to the adverse effects associated with their long-term use, such as brain volume loss and weight gain. In neurodegenerative diseases, antipsychotic-stimulated autophagy might help to increase the clearance and reduce neurotoxicity of aggregated proteotoxins. However, the possibility that some antipsychotics might block autophagic flux and potentially contribute to proteotoxin-mediated neurodegeneration must be considered. Finally, the anticancer effects of autophagy induction by antipsychotics make plausible their repurposing as adjuncts to standard cancer therapy.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vucicevic</LastName><ForeName>Ljubica</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Institute for Biological Research, University of Belgrade, Belgrade, Serbia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Misirkic-Marjanovic</LastName><ForeName>Maja</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institute for Biological Research, University of Belgrade, Belgrade, Serbia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Harhaji-Trajkovic</LastName><ForeName>Ljubica</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Institute for Biological Research, University of Belgrade, Belgrade, Serbia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maric</LastName><ForeName>Nadja</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Clinic of Psychiatry, Clinical Centre of Serbia and School of Medicine, University of Belgrade, Belgrade, Serbia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Trajkovic</LastName><ForeName>Vladimir</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Institute of Microbiology and Immunology, School of Medicine, University of Belgrade, Dr. Subotica 1, 11000 Belgrade, Serbia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>10</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>Austria</Country><MedlineTA>Cell Stress</MedlineTA><NlmUniqueID>101718867</NlmUniqueID><ISSNLinking>2523-0204</ISSNLinking></MedlineJournalInfo><CoiStatement>Conflict of interest: The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>6</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>6</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>6</Month><Day>22</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31225453</ArticleId><ArticleId IdType="doi">10.15698/cst2018.11.161</ArticleId><ArticleId IdType="pii">CST0178E139</ArticleId><ArticleId IdType="pmc">PMC6551804</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Expert Opin Pharmacother. 2001 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