ReviewCells2018
Mitochondrial Metabolism in Major Neurological Diseases.
Review in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed.
- Comparative Transcriptome Analysis Reveals Tissue-Specific Expression and Conservation of Mitochondrial Metal and Cofactor Genes in Buffalo.Cell biochemistry and biophysics · 2026Article
- Targeting TMEM175 in Lysosomal Physiology and Human Diseases.Current stem cell research & therapy · 2026Review
- Review
- UQCRC1 is a Key Pathogenic Determinant and Potential Therapeutic Target for Cognitive Impairment in Alzheimer's Disease.Molecular neurobiology · 2025Article
- Plasma proteomic analysis identifies proteins and pathways related to Alzheimer's risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Role of mitochondrial metabolism in ischemic stroke and natural products intervention.Molecular biology reports · 2025Review
- Super-resolution imaging informed scRNA sequencing analysis reveals the critical role of GDF15 in rejuvenating aged hematopoietic stem cells.Blood science (Baltimore, Md.) · 2025Article
- Attenuated PINK1 autophosphorylation play neuroprotective and anti-seizure roles in neonatal hypoxia.Scientific reports · 2025Article
- Therapeutic Approach to Epilepsy in Patients with Mitochondrial Diseases.Yonsei medical journal · 2025Review
- Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- Engineered Mitochondrial Transplantation as An Anti-Aging Therapy.Aging and disease · 2024Review
- Mitochondrial Quality Control via Mitochondrial Unfolded Protein Response (mtUPR) in Ageing and Neurodegenerative Diseases.Biomolecules · 2023Review
- Protective mechanisms of quercetin in neonatal rat brain injury induced by hypoxic-ischemic brain damage (HIBD).Food science & nutrition · 2023Article
- Transcriptomic Analyses of Neurotoxic Astrocytes Derived from Adult Triple Transgenic Alzheimer's Disease Mice.Journal of molecular neuroscience : MN · 2023Article
- Escalating Bi-Directional Feedback Loops between Proinflammatory Microglia and Mitochondria in Ageing and Post-Diagnosis of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Action of the Purinergic and Cholinergic Anti-inflammatory Pathways on Oxidative Stress in Patients with Alzheimer's Disease in the Context of the COVID-19 Pandemic.Neuroscience · 2023Review
- PHB2 affects the virulence of Vip3Aa to Sf9 cells through internalization and mitochondrial stability.Virulence · 2022Article
- Hydrogen-rich water ameliorates neuropathological impairments in a mouse model of Alzheimer's disease through reducing neuroinflammation and modulating intestinal microbiota.Neural regeneration research · 2022Article
- The mitochondrial proteomic changes of rat hippocampus induced by 28-day simulated microgravity.PloS one · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Mitochondria are bilayer sub-cellular organelles that are an integral part of normal cellular physiology. They are responsible for producing the majority of a cell's ATP, thus supplying energy for a variety of key cellular processes, especially in the brain. Although energy production is a key aspect of mitochondrial metabolism, its role extends far beyond energy production to cell signaling and epigenetic regulation⁻functions that contribute to cellular proliferation, differentiation, apoptosis, migration, and autophagy. Recent research on neurological disorders suggest a major metabolic component in disease pathophysiology, and mitochondria have been shown to be in the center of metabolic dysregulation and possibly disease manifestation. This review will discuss the basic functions of mitochondria and how alterations in mitochondrial activity lead to neurological disease progression.
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.