Zagrebelsky Marta, Korte Martin
Division of Cellular Neurobiology, Zoological Institute, TU Braunschweig, Braunschweig, Germany.
Neural Regen Res. 2024 Jan;19(1):29-34. doi: 10.4103/1673-5374.374138.
Brain-derived neurotrophic factor signaling via its receptor tropomyosin receptor kinase B regulates several crucial physiological processes. It has been shown to act in the brain, promoting neuronal survival, growth, and plasticity as well as in the rest of the body where it is involved in regulating for instance aspects of the metabolism. Due to its crucial and very pleiotropic activity, reduction of brain-derived neurotrophic factor levels and alterations in the brain-derived neurotrophic factor/tropomyosin receptor kinase B signaling have been found to be associated with a wide spectrum of neurological diseases. However, because of its poor bioavailability and pharmacological properties, brain-derived neurotrophic factor itself has a very low therapeutic value. Moreover, the concomitant binding of exogenous brain-derived neurotrophic factor to the p75 neurotrophin receptor has the potential to elicit several unwanted and deleterious side effects. Therefore, developing tools and approaches to specifically promote tropomyosin receptor kinase B signaling has become an important goal of translational research. Among the newly developed tools are different categories of tropomyosin receptor kinase B receptor agonist molecules. In this review, we give a comprehensive description of the different tropomyosin receptor kinase B receptor agonist drugs developed so far and of the results of their application in animal models of several neurological diseases. Moreover, we discuss the main benefits of tropomyosin receptor kinase B receptor agonists, concentrating especially on the new tropomyosin receptor kinase B agonist antibodies. The benefits observed both in vitro and in vivo upon application of tropomyosin receptor kinase B receptor agonist drugs seem to predominantly depend on their general neuroprotective activity and their ability to promote neuronal plasticity. Moreover, tropomyosin receptor kinase B agonist antibodies have been shown to specifically bind the tropomyosin receptor kinase B receptor and not p75 neurotrophin receptor. Therefore, while, based on the current knowledge, the tropomyosin receptor kinase B receptor agonists do not seem to have the potential to reverse the disease pathology per se, promoting brain-derived neurotrophic factor/tropomyosin receptor kinase B signaling still has a very high therapeutic relevance.
脑源性神经营养因子通过其受体原肌球蛋白受体激酶B发出的信号调节多个关键的生理过程。研究表明,它在大脑中发挥作用,促进神经元的存活、生长和可塑性,在身体其他部位也有作用,比如参与调节新陈代谢的各个方面。由于其关键且多效的活性,已发现脑源性神经营养因子水平的降低以及脑源性神经营养因子/原肌球蛋白受体激酶B信号的改变与多种神经系统疾病有关。然而,由于其生物利用度和药理性质较差,脑源性神经营养因子本身的治疗价值非常低。此外,外源性脑源性神经营养因子与p75神经营养因子受体的结合可能引发一些不良和有害的副作用。因此,开发特异性促进原肌球蛋白受体激酶B信号传导的工具和方法已成为转化研究的一个重要目标。新开发的工具中有不同类别的原肌球蛋白受体激酶B受体激动剂分子。在这篇综述中,我们全面描述了迄今为止开发的不同原肌球蛋白受体激酶B受体激动剂药物以及它们在几种神经系统疾病动物模型中的应用结果。此外,我们讨论了原肌球蛋白受体激酶B受体激动剂的主要益处,特别关注新型原肌球蛋白受体激酶B激动剂抗体。应用原肌球蛋白受体激酶B受体激动剂药物后在体外和体内观察到的益处似乎主要取决于它们的一般神经保护活性以及促进神经元可塑性的能力。此外,原肌球蛋白受体激酶B激动剂抗体已被证明能特异性结合原肌球蛋白受体激酶B受体,而不结合p75神经营养因子受体。因此,基于目前的知识,虽然原肌球蛋白受体激酶B受体激动剂本身似乎没有逆转疾病病理的潜力,但促进脑源性神经营养因子/原肌球蛋白受体激酶B信号传导仍然具有非常高的治疗相关性。