ArticleCell death & disease2019
The effect of fluoxetine on astrocyte autophagy flux and injured mitochondria clearance in a mouse model of depression.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
101 citing papers in PubMed, 4 syntheses or guidelines pooled it, 200 citations in OpenAlex.
- Mitochondrial-inflammation crosstalk in major depressive disorder: molecular mechanisms and therapeutic implications.Molecular psychiatry · 2026Pooled it
- Emerging Therapeutic Potential of Fluoxetine on Cognitive Decline in Alzheimer's Disease: Systematic Review.International journal of molecular sciences · 2024Pooled it
- Systematic review of Kaixinsan in treating depression: Efficacy and pharmacological mechanisms.Frontiers in behavioral neuroscience · 2022Pooled it
- The Association Between Antidepressant Effect of SSRIs and Astrocytes: Conceptual Overview and Meta-analysis of the Literature.Neurochemical research · 2021Pooled it
- Metformin Ameliorates Diabetes-Associated Cognitive Dysfunction via p53/Parkin-Mediated Mitophagy.Diabetes, obesity & metabolism · 2026Article
- Antidepressant Effects of 20-Glucoginsenoside Rf in an L-AAA-Induced Mouse Model with Glial-Associated Molecular Alterations.Current issues in molecular biology · 2026Article
- Exercise and fluoxetine in Alzheimer's disease: Molecular mechanisms of synergistic and antagonistic effects (Review).International journal of molecular medicine · 2026Review
- Human Stem Cell-Derived Neurospheroids and a Multi-Assay Strategy Provide Brain Cytotoxicity New Insights from ADB-FUBIATA Exposure.Neurotoxicity research · 2026Article
- Physical Activity and Depressive Mood Share the Structural Connectivity Between Motor and Reward Networks.Neuroscience bulletin · 2026Article
- Targeting ferroptosis as a novel strategy for depressive mental disorders.Psychopharmacology · 2026Review
- CircADAM9 activates autophagy via miR-302b-3p/ULK1 axis to improve depressive-like behaviors.Biology direct · 2026Article
- From energy metabolism to mood regulation: The rise of lactate as a therapeutic target.Journal of advanced research · 2026Review
- From mitochondrial oxidative stress to neuroinflammation: integrated proteomic and transcriptomic profiling reveals the role of the ROS/TXNIP/NLRP3 signaling pathway in anxious depression.Frontiers in immunology · 2026Article
- Effect of Venlafaxine on Inflammatory Level in Patients with Depression.Neuropsychiatric disease and treatment · 2026Article
- From metabolism to mood regulation: astrocytes as a driver of depression.Frontiers in cellular neuroscience · 2026Review
- Targeting the cGAS-STING Pathway: Modulating Inflammation, Oxidative Stress, and Autophagy for Novel Depression Therapies.Current neuropharmacology · 2026Review
- Pharmacological mechanisms of natural products with antidepressant effects: A focus on the programmed cell death regulation.Journal of pharmaceutical analysis · 2026Review
- Astrocytic SIRT1 ameliorates cognitive deficits after traumatic brain injury via autophagy-mediated MEGF10 phagocytosis.Journal of neuroinflammation · 2025Article
- Upregulated astrocytic HDAC7 induces depression-like disorders via deacetylating PINK1 and inhibiting mitophagy.Journal of neuroinflammation · 2025Article
- Distinct genetic responses to fluoxetine sertraline and citalopram in mouse cortical neurons.iScience · 2025Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although multiple hypotheses had been proposed to clarify the causes of depression, the accurate pathogenesis and effective treatment of depression still need to be solved. Pathological change of astrocytes has been recognized to play a pivotal role in depression. Fluoxetine is the first selective serotonin reuptake inhibitor, however, the underlying mechanisms of fluoxetine are incompletely excavated. Emerging evidence shows that fluoxetine promotes autophagic processes in tumor cells. However, whether astrocytic autophagy gets involved in the cytoprotection of fluoxetine on astrocytes in depression treatment remains unexplored. Here we prepared chronic mild stress (CMS)-induced mouse model and treated mice with fluoxetine (10 mg/kg) for 4 weeks to determine the correlation between proautophagic effect of fluoxetine and astrocyte protection in depression. Primary hippocampal astrocytes were cultured to investigate the potential mechanism of fluoxetine in regulating astrocyte autophagy. We found that fluoxetine (10 mg/kg) treatment promoted autophagosome formation and increased clearance of injured mitochondria, consequently protected astrocytes in CMS model mice. Fluoxetine (10 μM) could also promote the autophagic flux unblocked via enhancing fusion of autophagosomes with lysosomes in primary astrocytes. Moreover, fluoxetine promoted mitophagy by increased colocalization of autophagosomes and mitochondria, eliminating damaged mitochondria in corticosterone-treated astrocytes. Further in vitro study showed that p53 presence is required for fluoxetine activated autophagy flux and fluoxetine promotes astrocytic autophagy in a p53-dependent mechanism. Collectively, this work gives us insights into a novel approach to treat depression depending on astrocytes, and provides a promising molecular target for the development of antidepressant drugs besides regulating neurotransmitters.
Indexed as
Identifiers
What OpenQuestion holds
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.