PDF(Pubmed)
Abstract：
Although several methods are being applied to treat peripheral nerve injury, a perfect treatment that leads to full functional recovery has not yet been developed. SMAD (Suppressor of Mothers Against Decapentaplegic Homolog) plays a crucial role in nerve regeneration by facilitating the survival and growth of nerve cells following peripheral nerve injury. We conducted a systematic literature review on the role of SMAD in this context. Following peripheral nerve injury, there was an increase in the expression of SMAD1, -2, -4, -5, and -8, while SMAD5, -6, and -7 showed no significant changes; SMAD8 expression was decreased. Specifically, SMAD1 and SMAD4 were found to promote nerve regeneration, whereas SMAD2 and SMAD6 inhibited it. SMAD exerts its effects by promoting neuronal survival and growth through BMP/SMAD1, BMP/SMAD4, and BMP/SMAD7 signaling pathways. Furthermore, it activates nerve regeneration programs via the PI3K/GSK3/SMAD1 pathway, facilitating active regeneration of nerve cells and subsequent functional recovery after peripheral nerve damage. By leveraging these mechanisms of SMAD, novel strategies for treating peripheral nerve damage could potentially be developed. We aim to further elucidate the precise mechanisms of nerve regeneration mediated by SMAD and explore the potential for developing targeted nerve treatments based on these findings.
摘要：
虽然几种方法正在应用于治疗周围神经损伤，尚未开发出导致功能完全恢复的完美治疗方法。SMAD（母亲抗十一项截瘫同系物的抑制剂）通过促进周围神经损伤后神经细胞的存活和生长，在神经再生中起着至关重要的作用。我们对SMAD在这方面的作用进行了系统的文献综述。周围神经损伤后，SMAD1、-2、-4、-5和-8的表达增加，而SMAD5、-6和-7的表达无明显变化；SMAD8的表达减少。具体来说,SMAD1和SMAD4被发现促进神经再生，而SMAD2和SMAD6抑制它。SMAD通过BMP/SMAD1、BMP/SMAD4和BMP/SMAD7信号通路促进神经元存活和生长发挥其作用。此外，它通过PI3K/GSK3/SMAD1通路激活神经再生程序，促进神经细胞的主动再生和周围神经损伤后的功能恢复。通过利用SMAD的这些机制，有可能开发出治疗周围神经损伤的新策略.我们旨在进一步阐明SMAD介导的神经再生的确切机制，并基于这些发现探索开发靶向神经治疗的潜力。
