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Necrosis01:16

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Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
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Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
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Programmed NP Cell Death Induced by Mitochondrial ROS in a One-Strike Loading Disc Degeneration Organ Culture Model.

Bao-Liang Li1,2, Xizhe Liu2, Manman Gao3,4

  • 1Innovation Platform of Regeneration and Repair of Spinal Cord and Nerve Injury, Department of Orthopaedic Surgery, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen 518107, China.

Oxidative Medicine and Cellular Longevity
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This summary is machine-generated.

Mitochondrial reactive oxygen species (ROS) drive early cell death and matrix damage in degenerative disc disease after mechanical injury. Targeting ROS with MitoQ protects intervertebral discs from this damage.

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Area of Science:

  • Biomedical Engineering
  • Cell Biology
  • Orthopedics

Background:

  • Mechanical stress is a key factor in lumbar degenerative disc disease (DDD).
  • Mitochondrial reactive oxygen species (ROS) are implicated in DDD pathogenesis, but mechanisms require clarification.

Purpose of the Study:

  • To investigate the role of mitochondrial ROS in intervertebral disc (IVD) responses to mechanical stress.
  • To explore the therapeutic potential of targeting mitochondrial ROS in early DDD.

Main Methods:

  • A one-strike loading organ culture model of IVDs was used.
  • IVDs were subjected to mechanical strain and cultured with or without Mitoquinone mesylate (MitoQ).
  • Mitochondrial membrane potential, ROS levels, cell viability, apoptosis/necroptosis markers, and extracellular matrix (ECM) degeneration were assessed.

Main Results:

  • Mechanical stress rapidly decreased mitochondrial membrane potential and increased ROS levels and cell death markers within 12 hours.
  • MitoQ pretreatment significantly reduced ROS levels, improved cell viability, and mitigated early ECM degeneration.
  • Degenerative changes were most pronounced at early time points (12 hours) and resolved by day 7.

Conclusions:

  • Mitochondrial ROS are critical regulators of programmed nucleus pulposus cell death and ECM degeneration following mechanical injury in IVDs.
  • Targeting mitochondrial ROS with agents like MitoQ shows potential for preventing early-stage disc degeneration.