ReviewThe Journal of clinical investigation2019
Mitochondria, OxPhos, and neurodegeneration: cells are not just running out of gas.
Review in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.
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
93 citing papers in PubMed, 1 synthesis or guideline pooled it, 163 citations in OpenAlex.
- The complex interaction of genetics and delirium: a systematic review and meta-analysis.European archives of psychiatry and clinical neuroscience · 2021Pooled it
- A multi-organ spatial metabolomic atlas of exercising mice reveals neuronal Complex I as a convergent and sufficient axis for tau pathology reduction in PS19.bioRxiv : the preprint server for biology · 2026Article
- Pathogenic variants in the autophagy-tethering factor EPG5 drive neurodegeneration through mitochondrial dysfunction and innate immune activation.Nature communications · 2026Article
- Review
- Regulatory Variation at TERT and TERC Shows Limited Association with Early-Onset Alzheimer's Disease in Carriers of the Mexican Founder MutationMedical sciences (Basel, Switzerland) · 2026Article
- SIRT5-RNF126 coordinated regulation of METTL17 stability controls mitochondrial function and glioma progression.Cell & bioscience · 2026Article
- Dysfunction of mitochondria in intestinal epithelial cells: a key player in the pathogenesis of inflammatory bowel diseases.Gastroenterology report · 2026Review
- Cholesterol induced-mitochondrial calcium dysregulation facilitates atherosclerosis by promoting lipid accumulation in vascular smooth muscle cells.Molecular biomedicine · 2025Article
- Lithium nickel manganese cobalt oxide particles cause developmental neurotoxicity inEnvironmental science. Advances · 2025Article
- Mitochondrial dysfunction, a new marker warning of neuropsychiatric disorder risk: evidence from genetics and epidemiology.Annals of general psychiatry · 2025Article
- Dysregulation of cellular metabolism within the gut-brain axis is associated with behavioural changes in chronic intestinal inflammation.Journal of neuroinflammation · 2025Article
- Organic cation transporter 3 on neuronal mitochondria mediates MPPBMC biology · 2025Article
- Circ0515 reprogramming mitochondrial succinate metabolism and promotes lung adenocarcinoma progression through regulating SDHB.Cell death & disease · 2025Article
- Neural Metabolic Networks: Key Elements of Healthy Brain Function.Journal of neurochemistry · 2025Review
- The roles of mitochondria in global and local intracellular calcium signalling.Nature reviews. Molecular cell biology · 2025Review
- Article
- A novel polyribonucleotide nucleotidyltransferase 1 (Translational pediatrics · 2025Article
- The link between Mitochondria and Sarcopenia.Journal of physiology and biochemistry · 2025Review
- Altered mitochondria-associated ER membrane (MAM) function shifts mitochondrial metabolism in amyotrophic lateral sclerosis (ALS).Nature communications · 2025Article
- The Discovery of Phages in the Substantia Nigra and Its Implication for Parkinson's Disease.Research (Washington, D.C.) · 2025Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial respiratory deficiencies have been observed in numerous neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases. For decades, these reductions in oxidative phosphorylation (OxPhos) have been presumed to trigger an overall bioenergetic crisis in the neuron, resulting in cell death. While the connection between respiratory defects and neuronal death has never been proven, this hypothesis has been supported by the detection of nonspecific mitochondrial DNA mutations in these disorders. These findings led to the notion that mitochondrial respiratory defects could be initiators of these common neurodegenerative disorders, instead of being consequences of a prior insult, a theory we believe to be misconstrued. Herein, we review the roots of this mitochondrial hypothesis and offer a new perspective wherein mitochondria are analyzed not only from the OxPhos point of view, but also as a complex organelle residing at the epicenter of many metabolic pathways.
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.