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000140573 1001_ $$0P:(DE-2719)9001198$$aCavaliere, Federica$$b0$$eFirst author$$udzne
000140573 245__ $$aThe tricyclic antidepressant clomipramine inhibits neuronal autophagic flux.
000140573 260__ $$a[London]$$bMacmillan Publishers Limited, part of Springer Nature$$c2019
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000140573 520__ $$aAntidepressants 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.
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000140573 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x1
000140573 542__ $$2Crossref$$i2019-03-19$$uhttps://creativecommons.org/licenses/by/4.0
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000140573 650_2 $$2MeSH$$aAffective Disorders, Psychotic: drug therapy
000140573 650_2 $$2MeSH$$aAffective Disorders, Psychotic: pathology
000140573 650_2 $$2MeSH$$aAnimals
000140573 650_2 $$2MeSH$$aAntidepressive Agents, Tricyclic: adverse effects
000140573 650_2 $$2MeSH$$aAntidepressive Agents, Tricyclic: pharmacology
000140573 650_2 $$2MeSH$$aAutophagy: drug effects
000140573 650_2 $$2MeSH$$aCaenorhabditis elegans: drug effects
000140573 650_2 $$2MeSH$$aClomipramine: adverse effects
000140573 650_2 $$2MeSH$$aClomipramine: pharmacology
000140573 650_2 $$2MeSH$$aDisease Models, Animal
000140573 650_2 $$2MeSH$$aLiver: drug effects
000140573 650_2 $$2MeSH$$aLiver: metabolism
000140573 650_2 $$2MeSH$$aMice
000140573 650_2 $$2MeSH$$aNeurons: drug effects
000140573 650_2 $$2MeSH$$aNeurons: metabolism
000140573 650_2 $$2MeSH$$aNorepinephrine: metabolism
000140573 650_2 $$2MeSH$$aSerotonin: metabolism
000140573 650_2 $$2MeSH$$aSignal Transduction: drug effects
000140573 7001_ $$0P:(DE-2719)2690858$$aFornarelli, Alessandra$$b1
000140573 7001_ $$0P:(DE-2719)2810664$$aBertan, Fabio$$b2
000140573 7001_ $$aRusso, Rossella$$b3
000140573 7001_ $$0P:(DE-2719)2812207$$aMarsal Cots, Anais$$b4
000140573 7001_ $$aMorrone, Luigi Antonio$$b5
000140573 7001_ $$aAdornetto, Annagrazia$$b6
000140573 7001_ $$aCorasaniti, Maria Tiziana$$b7
000140573 7001_ $$0P:(DE-2719)2158358$$aBano, Daniele$$b8
000140573 7001_ $$aBagetta, Giacinto$$b9
000140573 7001_ $$0P:(DE-2719)2010732$$aNicotera, Pierluigi$$b10$$eLast author
000140573 77318 $$2Crossref$$3journal-article$$a10.1038/s41598-019-40887-x$$b : Springer Science and Business Media LLC, 2019-03-19$$n1$$p4881$$tScientific Reports$$v9$$x2045-2322$$y2019
000140573 773__ $$0PERI:(DE-600)2615211-3$$a10.1038/s41598-019-40887-x$$gVol. 9, no. 1, p. 4881$$n1$$p4881$$q9:1<4881$$tScientific reports$$v9$$x2045-2322$$y2019
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