Pan Xingli, Gao Yuxin, Guan Kaifu, Chen Jing, Ji Bingyuan
School of Biological Sciences, Jining Medical University, Jining 272067, China.
School of Clinical Medicine, Jining Medical University, Jining 272067, China.
Curr Issues Mol Biol. 2024 Jul 10;46(7):7324-7338. doi: 10.3390/cimb46070434.
Depression is the most common chronic mental illness and is characterized by low mood, insomnia, and affective disorders. However, its pathologic mechanisms remain unclear. Numerous studies have suggested that the ghrelin/GHSR system may be involved in the pathophysiologic process of depression. Ghrelin plays a dual role in experimental animals, increasing depressed behavior and decreasing anxiety. By combining several neuropeptides and traditional neurotransmitter systems to construct neural networks, this hormone modifies signals connected to depression. The present review focuses on the role of ghrelin in neuritogenesis, astrocyte protection, inflammatory factor production, and endocrine disruption in depression. Furthermore, ghrelin/GHSR can activate multiple signaling pathways, including cAMP/CREB/BDNF, PI3K/Akt, Jak2/STAT3, and p38-MAPK, to produce antidepressant effects, given which it is expected to become a potential therapeutic target for the treatment of depression.
抑郁症是最常见的慢性精神疾病，其特征为情绪低落、失眠和情感障碍。然而，其病理机制仍不清楚。大量研究表明，胃饥饿素/生长激素促分泌素受体（ghrelin/GHSR）系统可能参与抑郁症的病理生理过程。胃饥饿素在实验动物中发挥双重作用，增加抑郁行为并减轻焦虑。通过结合多种神经肽和传统神经递质系统来构建神经网络，这种激素会改变与抑郁症相关的信号。本综述重点关注胃饥饿素在抑郁症的神经突生成、星形胶质细胞保护、炎症因子产生和内分泌紊乱中的作用。此外，胃饥饿素/GHSR可激活多种信号通路，包括cAMP/CREB/BDNF、PI3K/Akt、Jak2/STAT3和p38-MAPK，以产生抗抑郁作用，鉴于此，它有望成为治疗抑郁症的潜在治疗靶点。
