This review highlights cardiovascular and immune dysfunction in cocaine users, suggesting emerging mechanisms beyond neurotransmitter dysregulation.
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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Darouiche et al. (2025) studied this question.
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