ReviewAutophagy2024
The beneficial role of autophagy in multiple sclerosis: Yes or No?
Review in Autophagy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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
47 citing papers in PubMed, 74 citations in OpenAlex.
- Emerging perspectives in proteostasis: bridging mechanisms and therapeutics for human diseases.Signal transduction and targeted therapy · 2026Review
- MCC950 suppresses NLRP3-dependent neuroinflammation and ameliorates cognitive decline in a rat model of cerebral small vessel disease.Neural regeneration research · 2026Article
- Role of Caveolin-1 in Inflammation: Genetic Predisposition and Potential Implication for Multiple Sclerosis.Genes · 2026Review
- Mechanism of action and clinical application of autophagy in multiple sclerosis (Review).International journal of molecular medicine · 2026Review
- Common molecular signatures: the role of BDNF, melatonin, and orexin in the ASD-schizophrenia continuum.Molecular biology reports · 2026Review
- Placental dysfunction, inflammation, and impaired autophagy in preeclampsia: A pathophysiological link to autism spectrum disorder.Metabolic brain disease · 2026Review
- SIRT1 Activators as Geroprotective Agents in Brain Aging: Mechanisms and Therapeutic Potential.Neuromolecular medicine · 2026Review
- The potential role of adenosinergic pathway and methylxanthines in Parkinson's disease: Blowing in the wind or not.Purinergic signalling · 2026Review
- Cell death in multiple sclerosis.Cell death and differentiation · 2026Review
- The potential role of COX-2/PGs signaling pathway in epileptogenesis and associated neuroinflammation: collusions or serendipity.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
- Thonningianin A derived from Penthorum chinense Pursh alleviates cerebral ischemia/reperfusion-mediated apoptosis and pyroptosis through the activation of PINK1/Parkin-dependent mitophagy.Chinese medicine · 2026Article
- Autophagy-NLRP3 Inflammasome Crosstalk in Microglia: A Therapeutic Target for Multiple Sclerosis.Inflammation · 2026Review
- Deciphering the Neuroautophagic Interactome: Molecular Circuits Linking Selective Autophagy to Neuropathological Cascades in Neurological Disorders.International journal of biological sciences · 2026Review
- Acupuncture regulates neuroinflammation: microglial glucose metabolism reprogramming as a potential mediating mechanism.Frontiers in immunology · 2026Review
- Post-onset intermittent fasting attenuates neuroinflammation and demyelination via a TRIB3-PERK-autophagy axis in an EAE model of multiple sclerosis.Journal of neuroinflammation · 2025Article
- "Rewiring brain immunity: targeting microglial metabolism for neuroprotection in neurodegenerative disorders".Metabolic brain disease · 2025Review
- Single-cell RNA sequencing of cerebrospinal fluid immune cells in relapsing-remitting multiple sclerosis: insights into cellular composition and immune dynamics.Journal of neurology · 2025Article
- Bridging the Gap: The Neuro-immune Axis as a Key Player in Neurodegenerative Disorders.Neuroscience bulletin · 2025Review
- Microglial Autophagy and Mitophagy in Ischemic Stroke: From Dual Roles to Therapeutic Modulation.Biology · 2025Review
- Glial Cytokine and Metabolic Networks in Progressive Multiple Sclerosis: From Pathophysiology to Biomarkers and Therapeutic Strategies.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
Abstract
Multiple sclerosis (MS) is a chronic progressive demyelinating disease of the central nervous system (CNS) due to an increase of abnormal peripherally auto-reactive T lymphocytes which elicit autoimmunity. The main pathophysiology of MS is myelin sheath damage by immune cells and a defect in the generation of myelin by oligodendrocytes. Macroautophagy/autophagy is a critical degradation process that eliminates dysfunctional or superfluous cellular components. Autophagy has the property of a double-edged sword in MS in that it may have both beneficial and detrimental effects on MS neuropathology. Therefore, this review illustrates the protective and harmful effects of autophagy with regard to this disease. Autophagy prevents the progression of MS by reducing oxidative stress and inflammatory disorders. In contrast, over-activated autophagy is associated with the progression of MS neuropathology and in this case the use of autophagy inhibitors may alleviate the pathogenesis of MS. Furthermore, autophagy provokes the activation of different immune and supporting cells that play an intricate role in the pathogenesis of MS. Autophagy functions in the modulation of MS neuropathology by regulating cell proliferation related to demyelination and remyelination. Autophagy enhances remyelination by increasing the activity of oligodendrocytes, and astrocytes. However, autophagy induces demyelination by activating microglia and T cells. In conclusion, specific autophagic activators of oligodendrocytes, and astrocytes, and specific autophagic inhibitors of dendritic cells (DCs), microglia and T cells induce protective effects against the pathogenesis of MS.
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.