Zhao Shuwu, Zhu Liping, Yang Jinfeng
Department of Anesthesiology, Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.
Department of Rehabilitation Medicine, The 3rd Xiangya Hospital, Central South University, Changsha, China.
Front Psychiatry. 2023 Jun 29;14:1215173. doi: 10.3389/fpsyt.2023.1215173. eCollection 2023.
Depression and macrovascular diseases are globally recognized as significant disorders that pose a substantial socioeconomic burden because of their associated disability and mortality. In addition, comorbidities between depression and macrovascular diseases have been widely reported in clinical settings. Patients afflicted with coronary artery disease, cerebrovascular disease or peripheral artery disease exhibit an elevated propensity for depressive symptoms. These symptoms, in turn, augment the risk of macrovascular diseases, thereby reflecting a bidirectional relationship. This review examines the physiological and pathological mechanisms behind comorbidity while also examining the intricate connection between depression and macrovascular diseases. The present mechanisms are significantly impacted by atypical activity in the hypothalamic-pituitary-adrenal axis. Elevated levels of cortisol and other hormones may disrupt normal endothelial cell function, resulting in vascular narrowing. At the same time, proinflammatory cytokines like interleukin-1 and C-reactive protein have been shown to disrupt the normal function of neurons and microglia by affecting blood-brain barrier permeability in the brain, exacerbating depressive symptoms. In addition, platelet hyperactivation or aggregation, endothelial dysfunction, and autonomic nervous system dysfunction are important comorbidity mechanisms. Collectively, these mechanisms provide a plausible physiological basis for the interplay between these two diseases. Interdisciplinary collaboration is crucial for future research aiming to reveal the pathogenesis of comorbidity and develop customised prevention and treatment strategies.
抑郁症和大血管疾病在全球范围内被公认为是重大疾病，因其相关的残疾和死亡率而带来巨大的社会经济负担。此外，抑郁症和大血管疾病之间的共病情况在临床环境中已被广泛报道。患有冠状动脉疾病、脑血管疾病或外周动脉疾病的患者出现抑郁症状的倾向更高。反过来，这些症状又增加了患大血管疾病的风险，从而反映出一种双向关系。本综述探讨了共病背后的生理和病理机制，同时也研究了抑郁症和大血管疾病之间的复杂联系。目前的机制受到下丘脑-垂体-肾上腺轴异常活动的显著影响。皮质醇和其他激素水平的升高可能会破坏正常的内皮细胞功能，导致血管狭窄。与此同时，白细胞介素-1和C反应蛋白等促炎细胞因子已被证明会通过影响大脑中的血脑屏障通透性来破坏神经元和小胶质细胞的正常功能，加重抑郁症状。此外，血小板过度活化或聚集、内皮功能障碍和自主神经系统功能障碍是重要的共病机制。总体而言，这些机制为这两种疾病之间的相互作用提供了一个合理的生理基础。跨学科合作对于未来旨在揭示共病发病机制并制定定制化预防和治疗策略的研究至关重要。
