ArticleMolecular psychiatry2023
BNIP3L/NIX-mediated mitophagy alleviates passive stress-coping behaviors induced by tumor necrosis factor-α.
Article in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.
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Who cites it
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.
- Mitochondrial-inflammation crosstalk in major depressive disorder: molecular mechanisms and therapeutic implications.Molecular psychiatry · 2026Pooled it
- Natural antidepressants in neuroimmunomodulation: molecular mechanisms, action targets, and therapeutic potential.Frontiers in immunology · 2025Pooled it
- Compensatory Mitophagy via NEDD4/HIF-1α/BNIP3 Pathway Restrains EndMT and Renal Allograft Interstitial Fibrosis Induced by TNFα.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitophagy in neuronal health and disease: from mechanisms to neurodegeneration.The Journal of clinical investigation · 2026Review
- Liver-derived complement component 3 promotes the susceptibility to stress-induced depression by impairing blood-brain barrier integrity.Molecular psychiatry · 2026Article
- Non-classical NMDAR subunit GluN3A in a specialized hippocampal region regulates stress-coping strategies in male mice.Communications biology · 2026Article
- The multifaceted functions of selective autophagy in cancer: molecular basis, consequences, and clinical prospects.Molecular cancer · 2026Review
- A Non-Mitophagy Activity of BNIP3L/NIX in Amygdala Glutamatergic Neurons is Essential for Contextual Fear Memory Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Wogonin Mitigates Depression by Inhibiting TNF-α/TNFR1/CXCL1 Signalling-Mediated Astrocyte Activation.Journal of cellular and molecular medicine · 2026Article
- Lipopolysaccharide Upregulates Neuroinflammation, Oxidative Stress Responses, and Peroxiredoxins in Depression Models.Brain and behavior · 2026Article
- Distinct effects of different Bacteroides strains on depressive-like behavior via a gut-Th1/Th17 cells-brain axis.Communications biology · 2026Article
- Investigating the Antidepressant Mechanism of Acupuncture with a Focus on Mitochondrial Homeostasis.International journal of general medicine · 2026Review
- Mental health and gut-brain crosstalk: implications for depression and Alzheimer's disease.Neuroscience applied · 2026Review
- Targeting the cGAS-STING Pathway: Modulating Inflammation, Oxidative Stress, and Autophagy for Novel Depression Therapies.Current neuropharmacology · 2026Review
- Intestinal γδ T17-IL-17A signaling disrupts hippocampal mitophagy in stress-induced depression and is restored by arketamine.Journal of neuroinflammation · 2025Article
- Pediococcus acidilactici attenuates chronic stress-induced depression via generating metabolite indole-3-lactic acid and downregulating neuroinflammation.Journal of neuroinflammation · 2025Article
- Molecular Links Between Metabolism and Mental Health: Integrative Pathways from GDF15-Mediated Stress Signaling to Brain Energy Homeostasis.International journal of molecular sciences · 2025Review
- Schisandrin C Improves Chronic Stress-Induced Dyslipidemia in Mice by Regulating Pyroptosis and Autophagy Levels.Journal of microbiology and biotechnology · 2025Article
- Review
- Chronic mild stress disrupts mitophagy and mitochondrial status in rat frontal cortex.Journal of translational medicine · 2025Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Recent studies based on animal models of various neurological disorders have indicated that mitophagy, a selective autophagy that eliminates damaged and superfluous mitochondria through autophagic degradation, may be involved in various neurological diseases. As an important mechanism of cellular stress response, much less is known about the role of mitophagy in stress-related mood disorders. Here, we found that tumor necrosis factor-α (TNF-α), an inflammation cytokine that plays a particular role in stress responses, impaired the mitophagy in the medial prefrontal cortex (mPFC) via triggering degradation of an outer mitochondrial membrane protein, NIP3-like protein X (NIX). The deficits in the NIX-mediated mitophagy by TNF-α led to the accumulation of damaged mitochondria, which triggered synaptic defects and behavioral abnormalities. Genetic ablation of NIX in the excitatory neurons of mPFC caused passive coping behaviors to stress, and overexpression of NIX in the mPFC improved TNF-α-induced synaptic and behavioral abnormalities. Notably, ketamine, a rapid on-set and long-lasting antidepressant, reversed the TNF-α-induced behavioral abnormalities through activation of NIX-mediated mitophagy. Furthermore, the downregulation of NIX level was also observed in the blood of major depressive disorder patients and the mPFC tissue of animal models. Infliximab, a clinically used TNF-α antagonist, alleviated both chronic stress- and inflammation-induced behavioral abnormalities via restoring NIX level. Taken together, these results suggest that NIX-mediated mitophagy links inflammation signaling to passive coping behaviors to stress, which underlies the pathophysiology of stress-related emotional disorders.
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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.