Mechanosensation in traumatic brain injury.
Mechanosensation in traumatic brain injury.
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DOI：
10.1016/j.nbd.2020.105210
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发表时间：
2021-01
影响因子：
6.1
通讯作者：
Cullen DK
中科院分区：
文献类型：
--
作者：
Keating CE;Cullen DK
创伤性脑损伤(TBI)不同于其他神经疾病，因为它是由对大脑施加极端机械力的离散事件引起的。这篇综述描述了大脑在正常情况下和受伤期间是如何感知、整合和反应外力的。对力的反应受到脑组织独特的机械特性的影响，这些特性因区域、细胞类型和亚细胞结构而不同。细胞外基质、质膜、跨膜受体和细胞骨架等元素影响其特性。这些相同的成分也起到力传感器的作用，使神经元和神经胶质细胞对物理环境做出反应，并保持动态平衡。然而，当外力变得太大时，如在颅脑损伤中，这些组件可能会以异常的方式反应或结构失效，导致独特的病理后遗症。这种所谓的“病理性机械感觉”代表了一系列细胞反应，这些反应随损伤的整体生物力学参数而变化，并可能因重复损伤而复杂化。这种对细胞的异常生理反应和/或损伤以及由此产生的继发性损伤级联反应最终会导致长期的细胞功能障碍和退化，通常会导致持续性的缺陷。事实上，病理机械感觉不仅直接启动继发性损伤级联反应，而且这种物理损伤后环境提供了这些级联反应展开的背景。总而言之，这些观点强调了使用准确复制人类脑外伤生物力学的实验模型的必要性。了解损伤生物力学背景下的细胞反应可能会揭示针对创伤特定后遗症的各个方面的治疗靶点。
Traumatic brain injury (TBI) is distinct from other neurological disorders because it is induced by a discrete event that applies extreme mechanical forces to the brain. This review describes how the brain senses, integrates, and responds to forces under both normal conditions and during injury. The response to forces is influenced by the unique mechanical properties of brain tissue, which differ by region, cell type, and subcellular structure. Elements such as the extracellular matrix, plasma membrane, transmembrane receptors, and cytoskeleton influences its properties. These same components also act as force-sensors, allowing neurons and glia to respond to their physical environment and maintain homeostasis. However, when applied forces become too large, as in TBI, these components may respond in an aberrant manner or structurally fail, resulting in unique pathological sequelae. This so-called “pathological mechanosensation” represents a spectrum of cellular responses, which vary depending on the overall biomechanical parameters of the injury and may be compounded by repetitive injuries. Such aberrant physical responses and/or damage to cells along with the resulting secondary injury cascades can ultimately lead to long-term cellular dysfunction and degeneration, often resulting in persistent deficits. Indeed, pathological mechanosensation not only directly initiates secondary injury cascades, but this post-physical damage environment provides the context in which these cascades unfold. Collectively, these points underscore the need to use experimental models that accurately replicate the biomechanics of TBI in humans. Understanding cellular responses in context with injury biomechanics may uncover therapeutic targets addressing various facets of trauma-specific sequelae.
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