Mahapatra Chitaranjan, Thakkar Ravindra, Kumar Ravinder
Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA 94158, USA.
California Institute for Quantitative Biosciences, University of California, Berkeley, CA 94720, USA.
Antioxidants (Basel). 2024 Sep 26;13(10):1172. doi: 10.3390/antiox13101172.
Oxidative stress, characterized by an imbalance between the production of reactive oxygen species (ROS) and the body's antioxidant defenses, significantly affects cellular function and viability. It plays a pivotal role in modulating membrane potentials, particularly action potentials (APs), essential for properly functioning excitable cells such as neurons, smooth muscles, pancreatic beta cells, and myocytes. The interaction between oxidative stress and AP dynamics is crucial for understanding the pathophysiology of various conditions, including neurodegenerative diseases, cardiac arrhythmias, and ischemia-reperfusion injuries. This review explores how oxidative stress influences APs, focusing on alterations in ion channel biophysics, gap junction, calcium dynamics, mitochondria, and Interstitial Cells of Cajal functions. By integrating current research, we aim to elucidate how oxidative stress contributes to disease progression and discuss potential therapeutic interventions targeting this interaction.
氧化应激以活性氧（ROS）生成与机体抗氧化防御之间的失衡为特征，显著影响细胞功能和活力。它在调节膜电位，尤其是动作电位（AP）方面起着关键作用，而动作电位对于神经元、平滑肌、胰腺β细胞和心肌细胞等可兴奋细胞的正常功能至关重要。氧化应激与AP动力学之间的相互作用对于理解包括神经退行性疾病、心律失常和缺血再灌注损伤在内的各种病症的病理生理学至关重要。本综述探讨氧化应激如何影响动作电位，重点关注离子通道生物物理学、缝隙连接、钙动力学、线粒体和 Cajal 间质细胞功能的改变。通过整合当前研究，我们旨在阐明氧化应激如何促进疾病进展，并讨论针对这种相互作用的潜在治疗干预措施。
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