Kentucky Spinal Cord Injury Research Center, University of Louisville School of Medicine, 511 S. Floyd St., MDR616, Louisville, KY 40202, USA.
Departments of Neurological Surgery, University of Louisville School of Medicine, 511 S. Floyd St., MDR616, Louisville, KY 40202, USA.
Cells. 2022 Oct 22;11(21):3339. doi: 10.3390/cells11213339.
Proteostasis (protein homeostasis) is critical for cellular as well as organismal survival. It is strictly regulated by multiple conserved pathways including the ubiquitin-proteasome system, autophagy, the heat shock response, the integrated stress response, and the unfolded protein response. These overlapping proteostasis maintenance modules respond to various forms of cellular stress as well as organismal injury. While proteostasis restoration and ultimately organism survival is the main evolutionary driver of such a regulation, unresolved disruption of proteostasis may engage pro-apoptotic mediators of those pathways to eliminate defective cells. In this review, we discuss proteostasis contributions to the pathogenesis of traumatic spinal cord injury (SCI). Most published reports focused on the role of proteostasis networks in acute/sub-acute tissue damage post-SCI. Those reports reveal a complex picture with cell type- and/or proteostasis mediator-specific effects on loss of neurons and/or glia that often translate into the corresponding modulation of functional recovery. Effects of proteostasis networks on such phenomena as neuro-repair, post-injury plasticity, as well as systemic manifestations of SCI including dysregulation of the immune system, metabolism or cardiovascular function are currently understudied. However, as potential interventions that target the proteostasis networks are expected to impact many cell types across multiple organ systems that are compromised after SCI, such therapies could produce beneficial effects across the wide spectrum of highly variable human SCI.
蛋白质稳态(protein homeostasis)对于细胞和机体的存活都至关重要。它受到多种保守途径的严格调控,包括泛素-蛋白酶体系统、自噬、热休克反应、综合应激反应和未折叠蛋白反应。这些重叠的蛋白质稳态维持模块可响应各种形式的细胞应激和机体损伤。虽然蛋白质稳态的恢复以及最终的机体存活是这种调节的主要进化驱动力,但蛋白质稳态的未解决破坏可能会使这些途径的促凋亡介质参与进来,以消除有缺陷的细胞。在这篇综述中,我们讨论了蛋白质稳态对创伤性脊髓损伤(SCI)发病机制的贡献。大多数已发表的报告都集中在蛋白质稳态网络在 SCI 后急性/亚急性组织损伤中的作用。这些报告揭示了一个复杂的情况,即细胞类型和/或蛋白质稳态介质对神经元和/或神经胶质细胞的丧失具有特异性影响,这通常转化为相应的功能恢复的调节。蛋白质稳态网络对神经修复、损伤后可塑性以及包括免疫系统、代谢或心血管功能失调在内的 SCI 的全身表现的影响目前研究较少。然而,由于预计靶向蛋白质稳态网络的潜在干预措施将影响 SCI 后多个受损器官系统中的许多细胞类型,因此这些治疗方法可能会对高度可变的人类 SCI 的广泛谱产生有益影响。