ArticleAntioxidants & redox signaling2014
Long-chain acyl coenzyme A synthetase 1 overexpression in primary cultured Schwann cells prevents long chain fatty acid-induced oxidative stress and mitochondrial dysfunction.
Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 56 citations in OpenAlex.
- Bioenergetic failure in diabetic peripheral neuropathy: from glucotoxicity to multidimensional metabolic imbalance.Journal of neurology · 2026Review
- Lipid alterations in hereditary peripheral neuropathies: common mechanisms in disease heterogeneity?Molecular neurodegeneration · 2026Review
- Bioorthogonal Probe BTD-Az Enables Sensitive and Rapid In Vivo Profiling of Protein Cysteine Sulfenylation.Bioconjugate chemistry · 2025Article
- Long-Chain Fatty Acids Alter Estrogen Receptor Expression in Breast Cancer Cells.International journal of molecular sciences · 2025Article
- Translating Basic Science to Clinical Applications: A Narrative Review of Repurposed Pharmacological Agents in Preclinical Models of Diabetic Neuropathy.Biomedicines · 2025Review
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- Diagnostic biomarker for type 2 diabetic peripheral neuropathy via comprehensive bioinformatics analysis.Journal of diabetes · 2024Article
- Immortalized Schwann cell lines as useful tools for pathogenesis-based therapeutic approaches to diabetic peripheral neuropathy.Frontiers in endocrinology · 2024Review
- New perspectives in diabetic neuropathy.Neuron · 2023Review
- Single-cell RNA-seq uncovers novel metabolic functions of Schwann cells beyond myelination.Journal of neurochemistry · 2023Article
- Cyclic stretch promotes vascular homing of endothelial progenitor cells via Acsl1 regulation of mitochondrial fatty acid oxidation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- New therapeutic directions in type II diabetes and its complications: mitochondrial dynamics.Frontiers in endocrinology · 2023Review
- The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications.Frontiers in endocrinology · 2023Review
- Nox, Nox, Are You There? The Role of NADPH Oxidases in the Peripheral Nervous System.Antioxidants & redox signaling · 2022Review
- A Role for Fatty Acids in Peripheral Neuropathy Associated with Type 2 Diabetes and Prediabetes.Antioxidants & redox signaling · 2022Review
- A novel ND1 mitochondrial DNA mutation is maternally inherited in growth hormone transgenesis in amago salmon (Oncorhynchus masou ishikawae).Scientific reports · 2022Article
- Molecular Aspects in the Potential of Vitamins and Supplements for Treating Diabetic Neuropathy.Current diabetes reports · 2021Review
- Transcriptomic Analysis of Human Mesenchymal Stem Cell Therapy in Incontinent Rat Injured Urethra.Tissue engineering. Part A · 2020Article
- Hepatic proteome analysis reveals altered mitochondrial metabolism and suppressed acyl-CoA synthetase-1 in colon-26 tumor-induced cachexia.Physiological genomics · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
aimsHigh circulating long chain fatty acids (LCFAs) are implicated in diabetic neuropathy (DN) development. Expression of the long-chain acyl-CoA synthetase 1 (Acsl1) gene, a gene required for LCFA metabolic activation, is altered in human and mouse diabetic peripheral nerve. We assessed the significance of Acsl1 upregulation in primary cultured Schwann cells.
resultsAcsl1 overexpression prevented oxidative stress (nitrotyrosine; hydroxyoctadecadienoic acids [HODEs]) and attenuated cellular injury (TUNEL) in Schwann cells following 12 h exposure to LCFAs (palmitate, linoleate, and oleate, 100 μM). Acsl1 overexpression potentiated the observed increase in medium to long-chain acyl-carnitines following 12 h LCFA exposure. Data are consistent with increased mitochondrial LCFA uptake, largely directed to incomplete beta-oxidation. LCFAs uncoupled mitochondrial oxygen consumption from ATP production. Acsl1 overexpression corrected mitochondrial dysfunction, increasing coupling efficiency and decreasing proton leak. INNOVATION: Schwann cell mitochondrial function is critical for peripheral nerve function, but research on Schwann cell mitochondrial dysfunction in response to hyperlipidemia is minimal. We demonstrate that high levels of a physiologically relevant mixture of LCFAs induce Schwann cell injury, but that improved mitochondrial uptake and metabolism attenuate this lipotoxicity.
conclusionAcsl1 overexpression improves Schwann cell function and survival following high LCFA exposure in vitro; however, the observed endogenous Acsl1 upregulation in peripheral nerve in response to diabetes is not sufficient to prevent the development of DN in murine models of DN. Therefore, targeted improvement in Schwann cell metabolic disposal of LCFAs may improve DN phenotypes.
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