ArticleScientific reports2019
The tricyclic antidepressant clomipramine inhibits neuronal autophagic flux.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Small-molecule autophagy modulators: Mechanisms, therapeutic potential, and development challenges in pathological settings.Fundamental research · 2026Review
- Clomipramine potentiates sorafenib efficacy in experimental hepatocellular carcinoma by targeting lysosomal sequestration and modulating the cathepsin B/Bcl-2/Beclin-1 axis.Molecular biology reports · 2026Article
- Targeting of Itch by clomipramine or gene therapy improves cognitive defects related to Alzheimer's disease.iScience · 2026Article
- Unlocking neuronal health: leveraging C. elegans for drug repurposing studies.Cell communication and signaling : CCS · 2026Review
- Enhancing clomipramine antidepressive effect using nanocomplexes via different routes of administration: A comparative study.Iranian journal of basic medical sciences · 2026Article
- Autophagy Modulation by Antidepressants: Mechanisms and Implications.Neurochemical research · 2025Review
- The Antidepressant Drug Amitriptyline Affects Human SH-SY5Y Neuroblastoma Cell Proliferation and Modulates Autophagy.International journal of molecular sciences · 2024Article
- Screening a neurotransmitter-receptor-related inhibitor library identifies clomipramine HCl as a potential antiviral compound against Japanese encephalitis virus.Infectious medicine · 2024Article
- FDA-approved drugs containing dimethylamine pharmacophore: a review of the last 50 years.RSC advances · 2024Review
- Tat-CCT2 Protects the Neurons from Ischemic Damage by Reducing Oxidative Stress and Activating Autophagic Removal of Damaged Protein in the Gerbil Hippocampus.Neurochemical research · 2023Article
- InhibitingPharmaceuticals (Basel, Switzerland) · 2023Article
- SGPL1 stimulates VPS39 recruitment to the mitochondria in MICU1 deficient cells.Molecular metabolism · 2022Article
- Virus-Induced Membrane Fusion in Neurodegenerative Disorders.Frontiers in cellular and infection microbiology · 2022Review
- Selective elimination of host cells harboring replication-competent human immunodeficiency virus reservoirs: a promising therapeutic strategy for HIV cure.Chinese medical journal · 2021Article
- Enriched environment boosts the post-stroke recovery of neurological function by promoting autophagy.Neural regeneration research · 2021Article
- The Unfolded Protein Response and Autophagy as Drug Targets in Neuropsychiatric Disorders.Frontiers in cellular neuroscience · 2020Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.