Naples James G
University of Connecticut Health Center, 263 Farmington Ave, Farmington, CT 06030, United States.
Med Hypotheses. 2017 Jul;104:121-125. doi: 10.1016/j.mehy.2017.05.036. Epub 2017 Jun 1.
Acquired sensorineural hearing loss represents a challenging clinical scenario. Currently, there are few approved therapies for treating this type of hearing loss, and diagnosis is often made after permanent damage has occurred. There are numerous etiologies for acquired hearing loss, with complex mechanisms underlying each cause. Despite these complexities, apoptosis of the structures within the inner ear, is a theme common to many forms of acquired hearing loss. Apoptosis is a calcium-dependent process, and within the inner ear, L- and T-type calcium channels are believed to contribute to calcium availability during this process. There are few studies limited to animal models evaluating the role of calcium-channel blockers (CCBs) as otoprotective agents in the setting of acquired hearing loss. Here, I hypothesize that CCBs will provide utility as a therapy against acquired forms of sensorineural hearing loss by preventing calcium influx that occurs during inner ear cellular apoptosis.
获得性感音神经性听力损失是一种具有挑战性的临床情况。目前，针对这类听力损失的获批疗法很少，而且往往在永久性损伤发生后才做出诊断。获得性听力损失有多种病因，每种病因背后都有复杂的机制。尽管存在这些复杂性，但内耳结构的凋亡是多种形式的获得性听力损失所共有的一个现象。凋亡是一个依赖钙的过程，在内耳中，L型和T型钙通道被认为在此过程中有助于钙的供应。很少有研究仅限于动物模型，评估钙通道阻滞剂（CCB）在获得性听力损失情况下作为耳保护剂的作用。在此，我假设CCB通过防止内耳细胞凋亡期间发生的钙内流，将作为一种治疗获得性感音神经性听力损失的疗法发挥作用。
