ArticleMolecular neurobiology2019
Lipotoxic Effects of Palmitic Acid on Astrocytes Are Associated with Autophagy Impairment.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 39 citations in OpenAlex.
- Docosahexaenoic Acid Protects Schwann Cells Against Palmitic Acid-Induced Lipotoxicity by Modulating Autophagy, ER Stress, and Lipid Handling.Neurochemical research · 2026Article
- Autophagy and metabolic homeostasis: Exploration in obesity‑related metabolic diseases (Review).International journal of molecular medicine · 2026Review
- Palmitic acid-induced autolysosomal dysfunction and lipotoxicity in neuroinflammation and neurodegeneration.Neural regeneration research · 2026Article
- Docosahexaenoic Acid Modulates Autophagy and Confers Neuronal Resilience under Hypoxia-Reoxygenation Stress.Journal of molecular neuroscience : MN · 2026Article
- Pro-Inflammatory Microglia Exacerbate High-Altitude-Induced Cognitive Impairment by Driving Lipid Droplet Accumulation in Astrocytes.Antioxidants (Basel, Switzerland) · 2025Article
- Palmitate-Induced Primary Rat Senescent Astrocytes Exhibit Higher Inflammatory Activity and a Distinct Transcriptomic Profile Compared to Reactive Astrocytes.Journal of neurochemistry · 2025Article
- Lysosomal acidification impairment in astrocyte-mediated neuroinflammation.Journal of neuroinflammation · 2025Review
- FECAL CALPROTECTIN AND INTESTINAL METABOLITES: WHAT IS THEIR IMPORTANCE IN THE ACTIVITY AND DIFFERENTIATION OF PATIENTS WITH INFLAMMATORY BOWEL DISEASES?Arquivos brasileiros de cirurgia digestiva : ABCD = Brazilian archives of digestive surgery · 2025Article
- Review on the role of hypothalamic astrocytes in the neuroendocrine control of metabolism.Journal of diabetes and metabolic disorders · 2024Review
- Article
- ANT-Mediated Inhibition of the Permeability Transition Pore Alleviates Palmitate-Induced Mitochondrial Dysfunction and Lipotoxicity.Biomolecules · 2024Article
- Enzymatic Metabolic Switches of Astrocyte Response to Lipotoxicity as Potential Therapeutic Targets for Nervous System Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Article
- Improvement in the prediction power of an astrocyte genome-scale metabolic model using multi-omic data.Frontiers in systems biology · 2024Article
- Elucidating glial responses to products of diabetes-associated systemic dyshomeostasis.Progress in retinal and eye research · 2023Review
- Profiling and Cellular Analyses of Obesity-Related circRNAs in Neurons and Glia under Obesity-like In Vitro Conditions.International journal of molecular sciences · 2023Article
- Competing endogenous RNAs in human astrocytes: crosstalk and interacting networks in response to lipotoxicity.Frontiers in neuroscience · 2023Article
- Modulation of Small RNA Signatures by Astrocytes on Early Neurodegeneration Stages; Implications for Biomarker Discovery.Life (Basel, Switzerland) · 2022Review
- Lipotoxicity as a Barrier for T Cell-Based Therapies.Biomolecules · 2022Review
- Tibolone Pre-Treatment Ameliorates the Dysregulation of Protein Translation and Transport Generated by Palmitic Acid-Induced Lipotoxicity in Human Astrocytes: A Label-Free MS-Based Proteomics and Network Analysis.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Obesity is associated with an increase in the brain levels of saturated free fatty acids, such as palmitic acid (PA). Previous studies have shown that PA exerts proinflammatory actions and reduces cell viability in astrocyte cultures. In this study, we have assessed whether an alteration in autophagy is involved in the effects of PA on astrocytes. Primary astrocytes were obtained from the cerebral cortex of male and female CD1 mouse pups and were incubated for 4.5 or 24 h with 250-500 μM PA. PA increased the levels of LC3-II, an autophagosome marker, and reduced LC3-II flux in astrocytes, suggesting a blockade of autophagy. This effect was observed both after 4.5 and 24 h of treatment with PA. PA had additional effects after treatment for 24 h, increasing the expression of proinflammatory cytokines, decreasing cell viability, and increasing the levels of an endoplasmic reticulum stress marker. In addition, PA decreased the expression of estrogen receptors, but only in female astrocytes. However, the treatment with estradiol, estrogen receptor agonists, or inhibitor of estradiol synthesis did not counteract the action of PA on cell viability. Rapamycin, an autophagy inducer, was unable to prevent the effect of PA on cell viability. In addition, hydroxychloroquine, an autophagy blocker, did not cause per se astrocyte death. These findings suggest that the effect of PA on autophagy is not sufficient to induce astrocyte loss, which is only observed when prolonged PA treatment causes other alterations in astrocytes, such as increased inflammation and endoplasmic reticulum stress.
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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.