Decoding Parkinson's Disease: The interplay of cell death pathways, oxidative stress, and therapeutic innovations

, ·OH), calcium dysregulation, and metabolic abnormalities, forming a self-amplifying vicious cycle. Non-neuronal cells (e.g., microglia and astrocytes) exacerbate neuronal redox damage by releasing pro-inflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β)), dysregulating iron/copper metabolism (enhancing Fenton chemistry), and suppressing autophagic flux. Therapeutic strategies targeting redox-critical nodes include caspase/RIPK1 inhibition, GPX4 activators, autophagy modulators (rapamycin), acid β-glucocerebrosidase (GBA1) restoration, iron/copper chelators, and antioxidants (N-acetylcysteine) to restore glutathione homeostasis. Additionally, regulating glial polarization…

• NN
  National Natural Science Foundation of China

  Awards: 81271410, 32161143021
• HU
  Henan University
• NS
  Natural Science Foundation of Henan Province

  Award: 182300410313
• HP
  Henan Province Science and Technology Innovation Talent Program

  Award: SYLYC2023092
• KR
  Key Research and Development Program of Hunan Province of China
• HP
  Henan Provincial Science and Technology Research Project

  Award: 231111311400