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<p>High glucose toxicity or hyperglycaemia manifests through various downstream processes, one of which is the elevation of oxidative stress. One of the consequences of increased reactive oxygen species production is mitochondrial damage, both metabolically and structurally. Arachidonic acid (AA) has been shown to salvage mitochondrial dysfunction in skeletal muscles. In this study, we explore the effects of lipoxin A4 (LXA4), a downstream anti-inflammatory metabolite of arachidonic acid, on mitigating hyperglycaemia-induced oxidative stress at the molecular level. We observed that LXA4 could substantially inhibit ROS production and restore Nrf2 expression (by 14%). Additionally, lipoxin A4 treatment was able to restore the mitochondrial potential and prevent mitochondrial fragmentation. Finally, due to the rescue of mitochondrial homeostasis and energetics, the process of myogenesis, an energy-extensive phenomenon, was also restored by the lipid treatment as evident from the differentiation parameters like myotube diameter and myonuclei fusion index, and the expression of MyoD, which drives the transition of myoblasts from proliferation to differentiation.</p> Graphical Abstract <p></p>

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Lipoxin A4 activates Nrf2 expression and mitigates hyperglycaemia-induced impairment of myogenesis and rescues damage to mitochondria

  • 期刊论文

  • 发表日期：

    2026年3月2日

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  • Akash Mitra,
  • Deepika Bhat. K,
  • Joel Rimson Pinto,
  • Samanwita Mandal,
  • Undurti Narasimha Das,
  • Bipasha Bose,
  • Sudheer Shenoy P

摘要

High glucose toxicity or hyperglycaemia manifests through various downstream processes, one of which is the elevation of oxidative stress. One of the consequences of increased reactive oxygen species production is mitochondrial damage, both metabolically and structurally. Arachidonic acid (AA) has been shown to salvage mitochondrial dysfunction in skeletal muscles. In this study, we explore the effects of lipoxin A4 (LXA4), a downstream anti-inflammatory metabolite of arachidonic acid, on mitigating hyperglycaemia-induced oxidative stress at the molecular level. We observed that LXA4 could substantially inhibit ROS production and restore Nrf2 expression (by 14%). Additionally, lipoxin A4 treatment was able to restore the mitochondrial potential and prevent mitochondrial fragmentation. Finally, due to the rescue of mitochondrial homeostasis and energetics, the process of myogenesis, an energy-extensive phenomenon, was also restored by the lipid treatment as evident from the differentiation parameters like myotube diameter and myonuclei fusion index, and the expression of MyoD, which drives the transition of myoblasts from proliferation to differentiation.

Graphical Abstract