可卡因诱导的心血管和免疫功能障碍:新出现的机制。

IF 10.3
Kyce Darouiche, Shelby Devin, Silvana Valdebenito, David Ajasin, Eliseo Eugenin
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引用次数: 0

摘要

物质使用及其相关合并症是一场影响数百万人的全球公共卫生危机,涉及合法和非法物质,包括可卡因、类阿片、甲基苯丙胺、芬太尼、酒精和大麻。目前,大多数药物滥用的研究都集中在药物介导的单胺能和谷氨酸能脑通路的失调上,因为它们在成瘾、耐受、依赖、戒断和复发中起作用。此外,使用可卡因的个体(娱乐性和慢性)也表现出外周损害的迹象,影响心血管系统、免疫功能和多种衰老过程。然而,潜在的机制仍然不完全清楚。最近,在非神经元细胞中描述了独立于神经递质失调的药物作用的新机制,这有助于解释药物使用者人群中心血管疾病、免疫损害和猝死的重大负担。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cocaine-Induced Cardiovascular and Immune Dysfunction: Emerging Mechanisms.

Substance use and its associated comorbidities are a global public health crisis affecting millions of people, involving both legal and illicit substances, including cocaine, opioids, methamphetamine, fentanyl, alcohol, and marijuana. Currently, most of the research in drug abuse has been focused on the drug-mediated dysregulation of the monoaminergic and glutamatergic brain pathways due to their role in addiction, tolerance, dependence, withdrawal, and relapse. In addition, individuals using cocaine (recreational and chronic) also exhibit signs of peripheral compromise, affecting the cardiovascular system, immune function, and multiple aging processes. However, the underlying mechanisms remain incompletely understood. Recently, emerging mechanisms of drug action, independent of neurotransmitter dysregulation, have been described in non-neuronal cells, helping to explain the significant burden of cardiovascular disease, immune compromise, and sudden death in the drug user population.

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