ReviewFrontiers in immunology2026
Focusing on microglial mitochondria-lysosome crosstalk and neuroinflammation underlying depression: from molecular pathways to potential therapeutic interventions.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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
1 citing paper in PubMed.
- Shared Immunogenetic Basis Between Spleen Volume and Psychiatric Disorders.Journal of molecular neuroscience : MN · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depression is a prevalent emotional disorder that significantly impacts global health. Its etiology is multifactorial, and current therapeutic options have notable limitations, underscoring the need to identify novel molecular targets and therapeutic strategies. Neuroinflammation is a key pathophysiological feature of depression, with microglia serving as innate immune cells in the central nervous system (CNS), playing a crucial role in neuroinflammation sensing and amplification. Mitochondria and lysosomes, which are responsible for energy metabolism and waste degradation, respectively, forms non-fusogenic interactions at mitochondrial-lysosomal contact sites (MLCs) in microglia, promoting physical contact and signal transduction, thereby modulating microglial metabolic states and inflammatory phenotypes. Disruption of MLCs can lead to reactive oxygen species (ROS) accumulation, enhanced pro-inflammatory cytokine production, and amplification of neuroinflammatory cascades, thereby accelerating the neuroinflammation-driven pathogenesis of depression. In this review, we focus on how microglial MLCs drive neuroinflammation and contribute to the pathophysiology of depression. First, this review explores how peripheral immune dysregulation, oxidative stress, and impaired autophagy initiate and sustain neuroinflammatory responses that exacerbate depressive behaviors. Then, this review elucidates how mitochondrial dysfunction and lysosomal pathology amplify inflammatory signaling and promote the progression of depressive neurobiology. It highlights microglial MLCs abnormalities as a crucial mechanistic hub, detailing how disrupted Ca²
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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 Socratic graph.