Stevens Andrew R, Belli Antonio, Ahmed Zubair
Institute of Inflammation and Ageing, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Centre for Trauma Sciences Research, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Biomedicines. 2024 Mar 13;12(3):643. doi: 10.3390/biomedicines12030643.
Traumatic injury to the brain and spinal cord (neurotrauma) is a common event across populations and often causes profound and irreversible disability. Pathophysiological responses to trauma exacerbate the damage of an index injury, propagating the loss of function that the central nervous system (CNS) cannot repair after the initial event is resolved. The way in which function is lost after injury is the consequence of a complex array of mechanisms that continue in the chronic phase post-injury to prevent effective neural repair. This review summarises the events after traumatic brain injury (TBI) and spinal cord injury (SCI), comprising a description of current clinical management strategies, a summary of known cellular and molecular mechanisms of secondary damage and their role in the prevention of repair. A discussion of current and emerging approaches to promote neuroregeneration after CNS injury is presented. The barriers to promoting repair after neurotrauma are across pathways and cell types and occur on a molecular and system level. This presents a challenge to traditional molecular pharmacological approaches to targeting single molecular pathways. It is suggested that novel approaches targeting multiple mechanisms or using combinatorial therapies may yield the sought-after recovery for future patients.
脑和脊髓的创伤性损伤(神经创伤)在人群中很常见,常常导致严重且不可逆转的残疾。对创伤的病理生理反应会加剧原发性损伤的损害,使中枢神经系统(CNS)在初始事件解决后无法修复的功能丧失进一步恶化。损伤后功能丧失的方式是一系列复杂机制的结果,这些机制在损伤后的慢性期持续存在,阻碍了有效的神经修复。本综述总结了创伤性脑损伤(TBI)和脊髓损伤(SCI)后的相关情况,包括对当前临床管理策略的描述、继发性损伤的已知细胞和分子机制及其在阻止修复中的作用的总结。还讨论了促进中枢神经系统损伤后神经再生的现有及新兴方法。神经创伤后促进修复的障碍存在于多种途径和细胞类型中,且发生在分子和系统层面。这给针对单一分子途径的传统分子药理学方法带来了挑战。建议针对多种机制的新方法或使用联合疗法可能为未来患者带来所期望的恢复。