ArticlePhilosophical transactions of the Royal Society of London. Series B, Biological sciences2020
Mitochondrial retrograde signalling in neurological disease.
Article in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Emerging perspectives on mitochondrial dysfunctioning and inflammation in epileptogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Pooled it
- Mitochondrial quality control in health and disease: Updates 2026.Chinese medical journal · 2026Review
- Nuclear translocation of mitochondrial ferredoxin reductase is regulated by AKT-mediated phosphorylation.The Biochemical journal · 2026Article
- Editorial: Mechanisms and novel therapeutic targets and approaches for mitochondrial dysfunction in neurological and cardiovascular diseases.Frontiers in physiology · 2026Article
- Mitochondrial DAMPs as a critical driver in the development of acute graft versus host disease and emerging mitochondria targeted therapeutic strategies.Frontiers in immunology · 2025Review
- Recent advances in mitochondria-targeting theranostic agents.Exploration (Beijing, China) · 2024Review
- A Drosophila model of mitochondrial disease phenotypic heterogeneity.Biology open · 2024Article
- Crosstalk between mitochondrial biogenesis and mitophagy to maintain mitochondrial homeostasis.Journal of biomedical science · 2023Review
- Yeast NDI1 reconfigures neuronal metabolism and prevents the unfolded protein response in mitochondrial complex I deficiency.PLoS genetics · 2023Article
- Adipose-Derived Mesenchymal Stem Cells Inhibit JNK-Mediated Mitochondrial Retrograde Pathway to Alleviate Acetaminophen-Induced Liver Injury.Antioxidants (Basel, Switzerland) · 2023Article
- Mitochondrial polymorphism m.3017C>T of SHLP6 relates to heterothermy.Frontiers in physiology · 2023Article
- Article
- Integrating cell morphology with gene expression and chemical structure to aid mitochondrial toxicity detection.Communications biology · 2022Article
- Nuclear-Mitochondrial Interactions.Biomolecules · 2022Review
- Article
- Decoding the rosetta stone of mitonuclear communication.Pharmacological research · 2020Review
- Retrograde signals from endosymbiotic organelles: a common control principle in eukaryotic cells.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal mitochondrial dysfunction causes primary mitochondrial diseases and likely contributes to neurodegenerative diseases including Parkinson's and Alzheimer's disease. Mitochondrial dysfunction has also been documented in neurodevelopmental disorders such as tuberous sclerosis complex and autism spectrum disorder. Only symptomatic treatments exist for neurodevelopmental disorders, while neurodegenerative diseases are largely untreatable. Altered mitochondrial function activates mitochondrial retrograde signalling pathways, which enable signalling to the nucleus to reprogramme nuclear gene expression. In this review, we discuss the role of mitochondrial retrograde signalling in neurological diseases. We summarize how mitochondrial dysfunction contributes to neurodegenerative disease and neurodevelopmental disorders. Mitochondrial signalling mechanisms that have relevance to neurological disease are discussed. We then describe studies documenting retrograde signalling pathways in neurons and glia, and in animal models of neuronal mitochondrial dysfunction and neurological disease. Finally, we suggest how specific retrograde signalling pathways can be targeted to develop novel treatments for neurological diseases. This article is part of the theme issue 'Retrograde signalling from endosymbiotic organelles'.
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.