ReviewBioscience reports2015
Mitochondrial dysfunction in fatty acid oxidation disorders: insights from human and animal studies.
Review in Bioscience reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.
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Who cites it
113 citing papers in PubMed, 228 citations in OpenAlex.
- ATAD3B and SKIL polymorphisms associated with antipsychotic-induced QTc interval change in patients with schizophrenia: a genome-wide association study.Translational psychiatry · 2022Trial
- Targeting glucagon signaling in metabolic disorders, functional insights from zebrafish receptor knockouts.Cellular and molecular life sciences : CMLS · 2026Article
- Targeting STAT3-mediated lipid metabolism reprogramming overcomes chemoresistance in acute myeloid leukemia.Cell death & disease · 2026Article
- Calpain-4 Knockdown Modulates Cholesterol Metabolism and LXRα Nuclear Localization in Experimental Alcohol-Related Liver Disease.Alcohol, clinical & experimental research · 2026Article
- Next-Generation Antioxidants in Cardiovascular Disease: Mechanistic Insights and Emerging Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Long-Chain Fatty Acid Oxidation Disorder Genes: A Comprehensive Genetic Database of LC-FAOD Variants, Genotypes, and Phenotypes.Human mutation · 2026Article
- Clinical spectrum and genotype-phenotype correlations ofFrontiers in neuroscience · 2026Article
- Comprehensive metabolomic characterization of patients with myasthenia gravis.Frontiers in immunology · 2026Article
- Dodecanedioic Acid: Alternative Carbon Substrate or Toxic Metabolite?Biomolecules · 2025Article
- Discovery of newborn Wilson disease biomarkers via integrated next-generation sequencing and untargeted metabolomics.Orphanet journal of rare diseases · 2025Article
- Beyond Bioenergetics: Emerging Roles of Mitochondrial Fatty Acid Oxidation in Stress Response and Aging.Cells · 2025Review
- Mitochondrial Dysfunction in the Cardiovascular Disease Continuum: Problems of Studying the Progression During the Follow-Up of the Pathologies.International journal of molecular sciences · 2025Review
- Article
- Calpain-4 Knockdown Modulates Cholesterol Metabolism and LXRα Nuclear Localization in Alcohol-Related Liver Disease.bioRxiv : the preprint server for biology · 2025Article
- Deletion of PTP1B in cardiomyocytes alters cardiac metabolic signaling to protect against cardiomyopathy induced by a high-fat diet.Science signaling · 2025Article
- Activating PPARβ/δ-Mediated Fatty Acid β-Oxidation Mitigates Mitochondrial Dysfunction Co-induced by Environmentally Relevant Levels of Molybdenum and Cadmium in Duck Kidneys.Biological trace element research · 2025Article
- Metabolomic Profiling of Ocular Fluid Identifies Host Response Factors for Risk Stratification in Bacterial Endophthalmitis.Investigative ophthalmology & visual science · 2025Article
- Mitochondrial Dysfunction and Atherosclerosis: The Problem and the Search for Its Solution.Biomedicines · 2025Review
- Untargeted Metabolomics Reveals Acylcarnitines as Major Metabolic Targets of Resveratrol in Breast Cancer Cells.Metabolites · 2025Article
- Metabolic abnormalities and reprogramming in cats with naturally occurring hypertrophic cardiomyopathy.ESC heart failure · 2025Article
53 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial fatty acid oxidation (FAO) plays a pivotal role in maintaining body energy homoeostasis mainly during catabolic states. Oxidation of fatty acids requires approximately 25 proteins. Inherited defects of FAO have been identified in the majority of these proteins and constitute an important group of inborn errors of metabolism. Affected patients usually present with severe hepatopathy, cardiomyopathy and skeletal myopathy, whereas some patients may suffer acute and/or progressive encephalopathy whose pathogenesis is poorly known. In recent years growing evidence has emerged indicating that energy deficiency/disruption of mitochondrial homoeostasis is involved in the pathophysiology of some fatty acid oxidation defects (FAOD), although the exact underlying mechanisms are not yet established. Characteristic fatty acids and carnitine derivatives are found at high concentrations in these patients and more markedly during episodes of metabolic decompensation that are associated with worsening of clinical symptoms. Therefore, it is conceivable that these compounds may be toxic. We will briefly summarize the current knowledge obtained from patients and genetic mouse models with these disorders indicating that disruption of mitochondrial energy, redox and calcium homoeostasis is involved in the pathophysiology of the tissue damage in the more common FAOD, including medium-chain acyl-CoA dehydrogenase (MCAD), long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) and very long-chain acyl-CoA dehydrogenase (VLCAD) deficiencies. We will also provide evidence that the fatty acids and derivatives that accumulate in these diseases disrupt mitochondrial homoeostasis. The elucidation of the toxic mechanisms of these compounds may offer new perspectives for potential novel adjuvant therapeutic strategies in selected disorders of this group.
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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.