ReviewCells2022
Mitochondrial Neurodegeneration.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 52 citations in OpenAlex.
- Placental mitochondrial DNA mutation-related oxidative stress underlies subsequent risk of adverse prognosis in sFGR twins.BMC pregnancy and childbirth · 2026Article
- Mitophagy: A key regulator in the pathophysiology and treatment of spinal cord injury.Neural regeneration research · 2026Article
- The impact of and changes in the oxidative status in the post-injury period following nonpenetrating traumatic brain injuries.The Journal of international medical research · 2026Article
- Hypoxic BMSC-derived exosomes-induced mitophagy quenches intestinal inflammation via HIF-1α/BNIP3 pathway.Scientific reports · 2025Article
- TMEM65-dependent Ca2+ extrusion safeguards mitochondrial homeostasis.Nature communications · 2025Article
- Dietary lipid content modifies wah-1/AIFM1-associated phenotypes via LRK-1 and DRP-1 expression in C. elegans.Nature communications · 2025Article
- The fourth family in the world with a novel variant in the ATP5MK gene: four siblings with complex V (ATP synthase) deficiency.Neurogenetics · 2025Article
- Mitochondrial complex I inhibition enhances astrocyte responsiveness to pro-inflammatory stimuli.Scientific reports · 2024Article
- A "one size fits all" gene therapy for neurological disorders with mitochondrial dysfunction.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Promoting Alzheimer's disease research and therapy with stem cell technology.Stem cell research & therapy · 2024Review
- Challenges and opportunities to bridge translational to clinical research for personalized mitochondrial medicine.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- Mitochondrial DNA Missense Mutations ChrMT: 8981A > G and ChrMT: 6268C > T Identified in a Caucasian Female with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) Triggered by the Epstein-Barr Virus.Case reports in genetics · 2024Article
- Decoding metabolic signatures in Alzheimer's disease: a mitochondrial perspective.Cell death discovery · 2023Review
- mtFociCounter for automated single-cell mitochondrial nucleoid quantification and reproducible foci analysis.Nucleic acids research · 2023Article
- The collective burden of childhood dementia: a scoping review.Brain : a journal of neurology · 2023Article
- The NADPH Link between the Renin Angiotensin System and the Antioxidant Mechanisms in Dopaminergic Neurons.Antioxidants (Basel, Switzerland) · 2023Review
- Brain washing and neural health: role of age, sleep, and the cerebrospinal fluid melatonin rhythm.Cellular and molecular life sciences : CMLS · 2023Review
- Neurodegeneration, Mitochondria, and Antibiotics.Metabolites · 2023Review
- Mitochondrial Neurodegeneration: Lessons fromBiomolecules · 2023Review
- Mitochondrial Transplantation in Mitochondrial Medicine: Current Challenges and Future Perspectives.International journal of molecular sciences · 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria are cytoplasmic organelles, which generate energy as heat and ATP, the universal energy currency of the cell. This process is carried out by coupling electron stripping through oxidation of nutrient substrates with the formation of a proton-based electrochemical gradient across the inner mitochondrial membrane. Controlled dissipation of the gradient can lead to production of heat as well as ATP, via ADP phosphorylation. This process is known as oxidative phosphorylation, and is carried out by four multiheteromeric complexes (from I to IV) of the mitochondrial respiratory chain, carrying out the electron flow whose energy is stored as a proton-based electrochemical gradient. This gradient sustains a second reaction, operated by the mitochondrial ATP synthase, or complex V, which condensates ADP and Pi into ATP. Four complexes (CI, CIII, CIV, and CV) are composed of proteins encoded by genes present in two separate compartments: the nuclear genome and a small circular DNA found in mitochondria themselves, and are termed mitochondrial DNA (mtDNA). Mutations striking either genome can lead to mitochondrial impairment, determining infantile, childhood or adult neurodegeneration. Mitochondrial disorders are complex neurological syndromes, and are often part of a multisystem disorder. In this paper, we divide the diseases into those caused by mtDNA defects and those that are due to mutations involving nuclear genes; from a clinical point of view, we discuss pediatric disorders in comparison to juvenile or adult-onset conditions. The complementary genetic contributions controlling organellar function and the complexity of the biochemical pathways present in the mitochondria justify the extreme genetic and phenotypic heterogeneity of this new area of inborn errors of metabolism known as 'mitochondrial medicine'.
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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.