Jarrahi Abbas, Braun Molly, Ahluwalia Meenakshi, Gupta Rohan V, Wilson Michael, Munie Stephanie, Ahluwalia Pankaj, Vender John R, Vale Fernando L, Dhandapani Krishnan M, Vaibhav Kumar
Department of Neurosurgery, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.
Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, WA 98195, USA.
Biomedicines. 2020 Sep 29;8(10):389. doi: 10.3390/biomedicines8100389.
Studying the complex molecular mechanisms involved in traumatic brain injury (TBI) is crucial for developing new therapies for TBI. Current treatments for TBI are primarily focused on patient stabilization and symptom mitigation. However, the field lacks defined therapies to prevent cell death, oxidative stress, and inflammatory cascades which lead to chronic pathology. Little can be done to treat the mechanical damage that occurs during the primary insult of a TBI; however, secondary injury mechanisms, such as inflammation, blood-brain barrier (BBB) breakdown, edema formation, excitotoxicity, oxidative stress, and cell death, can be targeted by therapeutic interventions. Elucidating the many mechanisms underlying secondary injury and studying targets of neuroprotective therapeutic agents is critical for developing new treatments. Therefore, we present a review on the molecular events following TBI from inflammation to programmed cell death and discuss current research and the latest therapeutic strategies to help understand TBI-mediated secondary injury.
研究创伤性脑损伤（TBI）所涉及的复杂分子机制对于开发TBI的新疗法至关重要。目前TBI的治疗主要集中在患者的稳定和症状缓解上。然而，该领域缺乏明确的疗法来预防导致慢性病理的细胞死亡、氧化应激和炎症级联反应。对于TBI原发性损伤期间发生的机械损伤几乎无能为力；然而，继发性损伤机制，如炎症、血脑屏障（BBB）破坏、水肿形成、兴奋性毒性、氧化应激和细胞死亡，可以通过治疗干预来靶向。阐明继发性损伤的多种潜在机制并研究神经保护治疗药物的靶点对于开发新疗法至关重要。因此，我们对TBI后从炎症到程序性细胞死亡的分子事件进行综述，并讨论当前的研究和最新的治疗策略，以帮助理解TBI介导的继发性损伤。
