Bipolar disorder is a decidedly heterogeneous and multifactorial disease, with a high individual and societal burden. While not all patients display overt markers of elevated inflammation, significant evidence suggests that aberrant immune signaling contributes to all stages of the disease, and likely explains the elevated rates of comorbid inflammatory illnesses seen in this population. While individual systems have been intensely studied and targeted, a relative paucity of attention has been given to the interconnecting role of inflammatory signals therein. This review presents an updated overview of some of the most prominent pathophysiologic mechanisms in bipolar disorder, from mitochondrial, endoplasmic reticular, and calcium homeostasis, to purinergic, kynurenic, and hormonal/neurotransmitter signaling, showing inflammation to act as a powerful nexus between these systems. Several areas with a high degree of mechanistic convergence within this paradigm are highlighted to present promising future targets for therapeutic development and screening.

中文翻译：

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双相情感障碍的炎症信号传导机制

双相情感障碍显然是一种异质性和多因素疾病，具有很高的个人和社会负担。虽然并非所有患者都表现出明显的炎症升高标志物，但重要证据表明，异常的免疫信号传导导致疾病的所有阶段，并可能解释了该人群中并发炎症性疾病发生率升高的原因。尽管对各个系统进行了深入研究和针对性研究，但对其中炎症信号的互连作用却相对缺乏关注。这篇综述对双相情感障碍中一些最重要的病理生理机制进行了更新概述，从线粒体、内质网和钙稳态，到嘌呤能、犬尿酸和激素/神经递质信号传导，表明炎症是这些系统之间的强大联系。强调了该范式中具有高度机械收敛性的几个领域，为治疗开发和筛选提出了有希望的未来目标。