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@ARTICLE{Cavaliere:140573,
      author       = {Cavaliere, Federica and Fornarelli, Alessandra and Bertan,
                      Fabio and Russo, Rossella and Marsal Cots, Anais and
                      Morrone, Luigi Antonio and Adornetto, Annagrazia and
                      Corasaniti, Maria Tiziana and Bano, Daniele and Bagetta,
                      Giacinto and Nicotera, Pierluigi},
      title        = {{T}he tricyclic antidepressant clomipramine inhibits
                      neuronal autophagic flux.},
      journal      = {Scientific reports},
      volume       = {9},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DZNE-2020-06895},
      pages        = {4881},
      year         = {2019},
      abstract     = {Antidepressants are commonly prescribed psychotropic
                      substances for the symptomatic treatment of mood disorders.
                      Their primary mechanism of action is the modulation of
                      neurotransmission and the consequent accumulation of
                      monoamines, such as serotonin and noradrenaline. However,
                      antidepressants have additional molecular targets that,
                      through multiple signaling cascades, may ultimately alter
                      essential cellular processes. In this regard, it was
                      previously demonstrated that clomipramine, a widely used
                      FDA-approved tricyclic antidepressant, interferes with the
                      autophagic flux and severely compromises the viability of
                      tumorigenic cells upon cytotoxic stress. Consistent with
                      this line of evidence, we report here that clomipramine
                      undermines autophagosome formation and cargo degradation in
                      primary dissociated neurons. A similar pattern was observed
                      in the frontal cortex and liver of treated mice, as well as
                      in the nematode Caenorhabditis elegans exposed to
                      clomipramine. Together, our findings indicate that
                      clomipramine may negatively regulate the autophagic flux in
                      various tissues, with potential metabolic and functional
                      implications for the homeostatic maintenance of
                      differentiated cells.},
      keywords     = {Affective Disorders, Psychotic: drug therapy / Affective
                      Disorders, Psychotic: pathology / Animals / Antidepressive
                      Agents, Tricyclic: adverse effects / Antidepressive Agents,
                      Tricyclic: pharmacology / Autophagy: drug effects /
                      Caenorhabditis elegans: drug effects / Clomipramine: adverse
                      effects / Clomipramine: pharmacology / Disease Models,
                      Animal / Liver: drug effects / Liver: metabolism / Mice /
                      Neurons: drug effects / Neurons: metabolism /
                      Norepinephrine: metabolism / Serotonin: metabolism / Signal
                      Transduction: drug effects},
      cin          = {AG Bano / AG Nicotera},
      ddc          = {600},
      cid          = {I:(DE-2719)1013003 / I:(DE-2719)5000018},
      pnm          = {341 - Molecular Signaling (POF3-341) / 342 - Disease
                      Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30890728},
      pmc          = {pmc:PMC6424961},
      doi          = {10.1038/s41598-019-40887-x},
      url          = {https://pub.dzne.de/record/140573},
}