ReviewInternational journal of molecular sciences2022
Depression Pathophysiology: Astrocyte Mitochondrial Melatonergic Pathway as Crucial Hub.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 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
13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.
- The Impact ofCurrent neuropharmacology · 2025Pooled it
- Bibliometric insights into astrocytic roles in depression and treatment.Frontiers in cellular neuroscience · 2024Pooled it
- Low Dose Ketamine Preconditions Astrocyte Mitochondria to Achieve Antidepressant Efficacy via Adenosine, Humanin, and Melatonin Upregulation and Efflux.Alpha psychiatry · 2026Article
- Peripheral metabolic-redox signaling as a core mechanism of major depressive disorder: evidence from deep metabolomic phenotyping.Acta neuropsychiatrica · 2026Article
- Dysfunctional circular RNA network in major depressive disorder: dissecting the cell identity and potential clinical applications.Molecular psychiatry · 2026Review
- Serotonergic Regulation in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Article
- Glucose Metabolic Abnormality: A Crosstalk between Depression and Alzheimer's Disease.Current neuropharmacology · 2025Review
- Mind-Body Medicine in the Treatment of Depression: A Narrative Review of Efficacy, Safety and Mechanisms.Current psychiatry reports · 2024Review
- Boltzmann's Theorem Revisited: Inaccurate Time-to-Action Clocks in Affective Disorders.Current neuropharmacology · 2024Review
- Review
- Type I Diabetes Pathoetiology and Pathophysiology: Roles of the Gut Microbiome, Pancreatic Cellular Interactions, and the 'Bystander' Activation of Memory CD8International journal of molecular sciences · 2023Review
- Melatonin, BAG-1 and cortisol circadian interactions in tumor pathogenesis and patterned immune responses.Exploration of targeted anti-tumor therapy · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Major depressive disorder (MDD) is widely accepted as having a heterogenous pathophysiology involving a complex mixture of systemic and CNS processes. A developmental etiology coupled to genetic and epigenetic risk factors as well as lifestyle and social process influences add further to the complexity. Consequently, antidepressant treatment is generally regarded as open to improvement, undoubtedly as a consequence of inappropriately targeted pathophysiological processes. This article reviews the diverse array of pathophysiological processes linked to MDD, and integrates these within a perspective that emphasizes alterations in mitochondrial function, both centrally and systemically. It is proposed that the long-standing association of MDD with suppressed serotonin availability is reflective of the role of serotonin as a precursor for the mitochondrial melatonergic pathway. Astrocytes, and the astrocyte mitochondrial melatonergic pathway, are highlighted as crucial hubs in the integration of the wide array of biological underpinnings of MDD, including gut dysbiosis and permeability, as well as developmental and social stressors, which can act to suppress the capacity of mitochondria to upregulate the melatonergic pathway, with consequences for oxidant-induced changes in patterned microRNAs and subsequent patterned gene responses. This is placed within a development context, including how social processes, such as discrimination, can physiologically regulate a susceptibility to MDD. Future research directions and treatment implications are derived from this.
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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.