ReviewCurrent neuropharmacology2019
Mitochondria: A Connecting Link in the Major Depressive Disorder Jigsaw.
Review in Current neuropharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 44 citations in OpenAlex.
- Targeting ferroptosis as a novel strategy for depressive mental disorders.Psychopharmacology · 2026Review
- The Role of Mitochondrial Dysfunction-Mediated Changes in Immune Cytokine Expression in the Pathophysiology and Treatment of Major Depressive Disorder.Molecular neurobiology · 2025Review
- An Updated Bio-Behavioral Profile of the Flinders Sensitive Line Rat: Reviewing the Findings of the Past Decade.Pharmacology research & perspectives · 2025Review
- Multi-omics investigation of metabolic dysregulation in depression: integrating metabolomics, weighted gene co-expression network analysis, and mendelian randomization.Frontiers in psychiatry · 2025Article
- Mitochondrial Dysfunction as a Biomarker of Illness State in Bipolar Disorder: A Critical Review.Brain sciences · 2024Review
- Major depressive disorder is associated with mitochondrialWorld journal of psychiatry · 2024Article
- Extremely Low-Frequency Electromagnetic Field (ELF-EMF) Increases Mitochondrial Electron Transport Chain Activities and Ameliorates Depressive Behaviors in Mice.International journal of molecular sciences · 2024Article
- CB1 receptor mediates anesthetic drug ketamine‑induced neuroprotection against glutamate in HT22 cells.Experimental and therapeutic medicine · 2024Article
- Serotonin regulation of mitochondria in kidney diseases.Pharmacological research · 2024Review
- Chronic stress dysregulates the Hippo/YAP/14-3-3η pathway and induces mitochondrial damage in basolateral amygdala in a mouse model of depression.Theranostics · 2024Article
- Resveratrol Attenuates Chronic Unpredictable Mild Stress-Induced Alterations in the SIRT1/PGC1α/SIRT3 Pathway and Associated Mitochondrial Dysfunction in Mice.Molecular neurobiology · 2023Article
- Therapeutic Potential of the Purinergic System in Major Depressive Disorder Associated with COVID-19.Cellular and molecular neurobiology · 2023Review
- Article
- Baicalin improves the energy levels in the prefrontal cortex of mice exposed to chronic unpredictable mild stress.Heliyon · 2022Article
- Metabolomics Based on Peripheral Blood Mononuclear Cells to Dissect the Mechanisms of Chaigui Granules for Treating Depression.ACS omega · 2022Article
- New Mechanisms and Targets of Subarachnoid Hemorrhage: A Focus on Mitochondria.Current neuropharmacology · 2022Review
- The Role of Mitochondria in Mood Disorders: From Physiology to Pathophysiology and to Treatment.Frontiers in psychiatry · 2021Review
- Clinical Evidence of Antidepressant Effects of Insulin and Anti-Hyperglycemic Agents and Implications for the Pathophysiology of Depression-A Literature Review.International journal of molecular sciences · 2020Review
- Advances in understanding mechanisms and therapeutic targets to treat comorbid depression and cardiovascular disease.Neuroscience and biobehavioral reviews · 2020Review
- Mangosteen Pericarp and Its Bioactive Xanthones: Potential Therapeutic Value in Alzheimer's Disease, Parkinson's Disease, and Depression with Pharmacokinetic and Safety Profiles.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDepression is a widespread phenomenon with varying degrees of pathology in different patients. Various hypotheses have been proposed for the cause and continuance of depression. Some of these include, but not limited to, the monoamine hypothesis, the neuroendocrine hypothesis, and the more recent epigenetic and inflammatory hypotheses.
objectiveIn this article, we review all the above hypotheses with a focus on the role of mitochondria as the connecting link. Oxidative stress, respiratory activity, mitochondrial dynamics and metabolism are some of the mitochondria-dependent factors which are affected during depression. We also propose exogenous ATP as a contributing factor to depression.
resultLiterature review shows that pro-inflammatory markers are elevated in depressive individuals. The cause for elevated levels of cytokines in depression is not completely understood. We propose exogenous ATP activates purinergic receptors which in turn increase the levels of various proinflammatory factors in the pathophysiology of depression.
conclusionMitochondria are integral to the function of neurons and undergo dysfunction in major depressive disorder patients. This dysfunction is reflected in all the various hypotheses that have been proposed for depression. Among the newer targets identified, which also involve mitochondria, includes the role of exogenous ATP. The diversity of purinergic receptors, and their differential expression among various individuals in the population, due to genetic and environmental (prenatal) influences, may influence the susceptibility and severity of depression. Identifying specific receptors involved and using patient-specific purinergic receptor antagonist may be an appropriate therapeutic course in the future.
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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.