发病机制
炎症
嘌呤能受体
免疫学
受体
细胞外
疾病
医学
嘌呤能信号
生物
细胞生物学
病理
腺苷受体
内科学
兴奋剂
作者
Natalia Rodriguez,Trinisia Fortune,Thien Vuong,Talia H. Swartz
标识
DOI:10.1016/j.coph.2023.102358
摘要
Human Immunodeficiency Virus Type 1 (HIV-1) causes a chronic, incurable infection associated with chronic inflammation despite virologic suppression on antiretroviral therapy (ART). This chronic inflammation underlies significant comorbidities, including cardiovascular disease, neurocognition decline, and malignancies. The mechanisms of chronic inflammation have been attributed, in part, to the role of extracellular ATP and P2X-type purinergic receptors that sense damaged or dying cells and undergo signaling responses to activate inflammation and immunomodulation. This review describes the current literature on the role of extracellular ATP and P2X receptors in HIV-1 pathogenesis, describing the known intersection with the HIV-1 life cycle in mediating immunopathogenesis and neuronal disease. The literature supports key roles for this signaling mechanism in cell-to-cell communication and in activating transcriptional changes that impact the inflammatory state leading to disease progression. Future studies must characterize the numerous functions of ATP and P2X receptors in HIV-1 pathogenesis to inform future therapeutic targeting.
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