细胞内和细胞外环境的失调以及细胞膜上离子通道的异常表达与各种退行性疾病密切相关。包括椎间盘退变.这种情况是腰痛的重要原因,这对个人生活质量和社会经济学都构成了沉重负担。离子通道的数量和功能的变化会破坏细胞内外的水和离子平衡,从而影响组织和器官的生理功能。因此,维持细胞微环境中的离子稳态和离子通道的稳定表达可能证明对治疗椎间盘退变有益。水通道蛋白(AQP),钙离子通道,和酸敏感离子通道(ASIC)在调节水,钙离子,和氢离子水平。这些通道对细胞衰老等生理和病理过程有显著影响,炎症反应,基质分解,内质网应激,和细胞代谢产物的积累。此外,压电1,瞬时受体电位香草素4型(TRPV4),张力反应增强子结合蛋白(TonEBP),钾离子,锌离子,和钨都在椎间盘退变过程中发挥作用。这篇综述试图阐明椎间盘退变(IVDD)时髓核微环境的改变,以期为探索针对椎间盘退变的治疗干预措施提供新的见解和方法。
The dysregulation of intracellular and extracellular environments as well as the aberrant expression of ion channels on the cell membrane are intricately linked to a diverse array of degenerative disorders, including intervertebral disc degeneration. This condition is a significant contributor to low back pain, which poses a substantial burden on both personal quality of life and societal economics. Changes in the number and function of ion channels can disrupt the water and ion balance both inside and outside cells, thereby impacting the physiological functions of tissues and organs. Therefore, maintaining ion homeostasis and stable expression of ion channels within the cellular microenvironment may prove beneficial in the treatment of disc degeneration. Aquaporin (AQP), calcium ion channels, and acid-sensitive ion channels (
ASIC) play crucial roles in regulating water, calcium ions, and hydrogen ions levels. These channels have significant effects on physiological and pathological processes such as cellular aging, inflammatory response, stromal decomposition, endoplasmic reticulum stress, and accumulation of cell metabolites. Additionally, Piezo 1, transient receptor potential vanilloid type 4 (TRPV4), tension response enhancer binding protein (TonEBP), potassium ions, zinc ions, and tungsten all play a role in the process of intervertebral disc degeneration. This review endeavors to elucidate alterations in the microenvironment of the nucleus pulposus during intervertebral disc degeneration (IVDD), with a view to offer novel insights and approaches for exploring therapeutic interventions against disc degeneration.