ReviewJournal of inherited metabolic disease2015
Redox signalling and mitochondrial stress responses; lessons from inborn errors of metabolism.
Review in Journal of inherited metabolic disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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.
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Who cites it
36 citing papers in PubMed, 75 citations in OpenAlex.
- Plasma metabolomics in infancy reveals early signatures of a stringently-defined otitis-prone phenotype.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026Article
- Mitochondria as an Integrative Hub of Cellular Homeostasis and Stress Response.International journal of molecular sciences · 2026Review
- Children's health: insights from space medicine on metabolic health.NPJ microgravity · 2025Review
- Article
- Mitochondrial diseases: from molecular mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Oxidative damage and mitochondrial dysfunction in cystathionine beta-synthase deficiency.Scientific reports · 2024Article
- Human inborn errors of long-chain fatty acid oxidation show impaired inflammatory responses to TLR4-ligand LPS.FASEB bioAdvances · 2024Article
- The bridge between cell survival and cell death: reactive oxygen species-mediated cellular stress.EXCLI journal · 2023Review
- Arginase 1 Deficiency in Patients Initially Diagnosed with Hereditary Spastic Paraplegia.Movement disorders clinical practice · 2023Review
- Role of FOXO3a Transcription Factor in the Regulation of Liver Oxidative Injury.Antioxidants (Basel, Switzerland) · 2022Review
- Mitochondrial Dysfunction and Redox Homeostasis Impairment as Pathomechanisms of Brain Damage in Ethylmalonic Encephalopathy: Insights from Animal and Human Studies.Cellular and molecular neurobiology · 2022Review
- An energetics perspective on geroscience: mitochondrial protonmotive force and aging.GeroScience · 2021Article
- Role of Melatonin in Angiotensin and Aging.Molecules (Basel, Switzerland) · 2021Review
- Mitochondria Content and Activity Are Crucial Parameters for Bull Sperm Quality Evaluation.Antioxidants (Basel, Switzerland) · 2021Article
- Effect of Proline on Cell Death, Cell Cycle, and Oxidative Stress in C6 Glioma Cell Line.Neurotoxicity research · 2021Article
- Cellular prion protein dysfunction in a prototypical inherited metabolic myopathy.Cellular and molecular life sciences : CMLS · 2021Article
- Increased antioxidant response in medium-chain acyl-CoA dehydrogenase deficiency: does lipoic acid have a protective role?Pediatric research · 2020Article
- Flavonoids and Mitochondria: Activation of Cytoprotective Pathways?Molecules (Basel, Switzerland) · 2020Review
- Physiopathological Bases of the Disease Caused byJournal of clinical medicine · 2020Article
- Enhanced mitochondrial biogenesis is associated with the ameliorative action of creatine supplementation in rat soleus and cardiac muscles.Experimental and therapeutic medicine · 2020Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria play a key role in overall cell physiology and health by integrating cellular metabolism with cellular defense and repair mechanisms in response to physiological or environmental changes or stresses. In fact, dysregulation of mitochondrial stress responses and its consequences in the form of oxidative stress, has been linked to a wide variety of diseases including inborn errors of metabolism. In this review we will summarize how the functional state of mitochondria -- and especially the concentration of reactive oxygen species (ROS), produced in connection with the respiratory chain -- regulates cellular stress responses by redox regulation of nuclear gene networks involved in repair systems to maintain cellular homeostasis and health. Based on our own and other's studies we re-introduce the ROS triangle model and discuss how inborn errors of mitochondrial metabolism, by production of pathological amounts of ROS, may cause disturbed redox signalling and induce chronic cell stress with non-resolving or compromised cell repair responses and increased susceptibility to cell stress induced cell death. We suggest that this model may have important implications for those inborn errors of metabolism, where mitochondrial dysfunction plays a major role, as it allows the explanation of oxidative stress, metabolic reprogramming and altered signalling growth pathways that have been reported in many of the diseases. It is our hope that the model may facilitate novel ideas and directions that can be tested experimentally and used in the design of future new approaches for pre-symptomatic diagnosis and prognosis and perhaps more effective treatments of inborn errors of metabolism.
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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.