中国神经再生研究(英文版) ›› 2025, Vol. 20 ›› Issue (3): 808-810.doi: 10.4103/NRR.NRR-D-24-00172

• 观点:退行性病与再生 • 上一篇    下一篇

瞬时受体电位通道与钙失调:帕金森病的致病二者

  

  • 出版日期:2025-03-15 发布日期:2024-06-26

Transient receptor potential channels and calcium dysregulation: a pathogenic duo in Parkinson’s disease

Iqira Saeed, Linlin Ma*   

  1. Griffith Institute for Drug Discovery, Griffith University, Nathan, Brisbane, QLD, Australia (Saeed I, Ma L)
    School of Environment and Science, Griffith University Nathan, Brisbane, QLD, Australia (Ma L)
  • Online:2025-03-15 Published:2024-06-26
  • Contact: Linlin Ma, PhD,linlin.ma@griffith.edu.au.

摘要: https://orcid.org/0000-0002-4716-5158 (Linlin Ma)

Abstract: Parkinson’s disease (PD) has a complex and multifactorial pathophysiology. Various studies, conducted both in pre-clinical models and PD patients, have reported a link between the disruption of calcium (Ca2+) homeostasis and the subsequent development of PD. Ca2+ regulation is crucial for neuronal survival, differentiation, exocytosis at synapses, gene transcription, and proliferation. In PD, disturbances in calcium homeostasis have been correlated with the selective degeneration of dopaminergic neurons within the substantia nigra pars compacta (SNpc), compared to neurons within other regions of the brain. More recently, there has been growing evidence to support the contribution of transient receptor potential (TRP) channels in calcium-mediated excitotoxicity and oxidative stress-induced death of dopaminergic neurons in PD.