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Related Concept Videos

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The ability of induced pluripotent stem cells or iPSCs to differentiate into most body cell types has stimulated repair and regenerative medicine research over the past few decades. iPSC-derived blood cells, hepatocytes, beta islet cells, cardiomyocytes, neurons, and other cell types can repair injuries or regenerate damaged tissue in diseases such as diabetes and neurodegenerative disorders.
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Author Spotlight: Advancing Hepatocyte Purification from Human Induced Pluripotent Stem Cells for Regenerative Medicine
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iPSC-Derived Hepatocytes from Patients with MASLD Exhibit Early Mitochondrial Dysfunction.

Dounia Le Guillou, Kevin Siao, Chris L Her

    Biorxiv : the Preprint Server for Biology
    |September 5, 2025
    PubMed
    Summary

    Metabolic dysfunction-associated steatotic liver disease (MASLD) patient cells show impaired mitochondria. These cells, when differentiated, exhibit lipid accumulation and reduced energy production, indicating early-stage liver disease.

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    Area of Science:

    • Hepatology
    • Mitochondrial Biology
    • Stem Cell Research

    Background:

    • Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by impaired hepatocyte mitochondrial adaptation to lipids.
    • Mitochondrial dysfunction in MASLD contributes to reactive oxygen species (ROS) production and disease progression.
    • Investigating mitochondrial function in patient-derived cells offers insights into early disease mechanisms.

    Purpose of the Study:

    • To determine if induced pluripotent stem cells (iPSCs) from MASLD patients, differentiated into hepatocyte-like cells (iPSC-Heps), display mitochondrial dysfunction.
    • To assess lipid accumulation, mitochondrial function, and cellular energy status in MASLD iPSC-Heps.
    • To explore the role of PNPLA3 genotype in MASLD-associated mitochondrial alterations.

    Main Methods:

    • Differentiated iPSCs from 10 MASLD patients and 10 healthy controls into iPSC-Heps.
    • Assessed mitochondrial mass and function under basal and palmitate-challenged conditions.
    • Measured gene expression, oxygen consumption, ROS production, and ATP levels.

    Main Results:

    • MASLD iPSC-Heps accumulated more lipids than controls.
    • Mitochondrial content was similar, but MASLD iPSC-Heps showed reduced oxygen consumption with palmitate.
    • MASLD iPSC-Heps exhibited increased ROS production and decreased ATP levels post-palmitate treatment.
    • These mitochondrial differences were independent of PNPLA3 genotype.

    Conclusions:

    • MASLD patient-derived iPSC-Heps recapitulate mitochondrial dysfunction observed in early MASLD.
    • The observed mitochondrial alterations precede the progression to steatohepatitis.
    • Mitochondrial dysfunction in this model is not solely dependent on the PNPLA3 genotype.