ArticleCureus2026
Involvement of Lysosomal Dysfunction and Its Association With Lipotoxic Stress in Palmitate-Treated HepG2 Cells.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- A Standardized Onion Peel-Derived Bioactive Ingredient Attenuates Palmitate-Induced Steatosis and Oxidative Stress by Modulating Mitochondrial Dynamics and Autophagy in HepG2 Cells.Antioxidants (Basel, Switzerland) · 2026Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction Nonalcoholic fatty liver disease (NAFLD), characterized by excessive lipid accumulation in the liver, is a growing global health burden. However, the intracellular events contributing to lipid-related liver injury remain incompletely defined. This study investigated the temporal association of lipotoxic events in HepG2 cells exposed to palmitic acid (PA). Methods A time course experiment was conducted to evaluate the effects of lipotoxicity on HepG2 cells. Intracellular reactive oxygen species (ROS), lysosomal destabilization, change in mitochondrial membrane potential (MMP), and cell death were assessed using a fluorescence spectrophotometer and a flow cytometer. Results Intracellular lipid accumulation and elevated ROS were detected shortly after PA exposure, followed by later alterations in redox balancecompared with control cells. As treatment progressed, significant lysosomal destabilization became evident from 18 hours onwards, leading to the increased cytosolic level and activity of cysteine protease, cathepsin B, into the cytosol. This lysosomal destabilization was associated with mitochondrial dysfunction, assessed by loss of MMP and release of cytochrome c (Cytc) from mitochondria. These events coincided with increased BAX expression, caspase 3 activation, and ultimately resulted in cell death. Importantly, pretreatment with bafilomycin A1 (BAF) markedly attenuated PA-related lysosomal destabilization, prevented cathepsin B activation, and reduced cell death, whereas a contrasting response was observed with chloroquine (CHQ) pretreatment. Together, these findings support a contributory role of lysosomal dysfunction in PA-associated lipotoxic stress. Conclusion This study outlines the temporal sequence of organelle dysfunction during PA-associated lipotoxicity and highlights the association of lysosomal impairment in NAFLD pathogenesis. Rather than serving as an upstream trigger, lysosomal impairment appears to function as a late-stage integrator of lipotoxic stress in this in-vitro HepG2 cells model.
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