受体丝氨酸/苏氨酸蛋白激酶 1 (RIPK1) 在艾滋病患者 CD4+ T 细胞坏死中的作用:文献综述

Asima Juliyana Siregar, Harun Hudari
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引用次数: 0

摘要

人类免疫缺陷病毒(HIV)能够消耗 CD4+ T 细胞,导致获得性免疫缺陷综合症(艾滋病),因此它仍然是全球健康的一大挑战。虽然凋亡在 CD4+ T 细胞耗竭中已被广泛研究,但最近的研究强调了坏死(一种受调控的坏死形式)在这一过程中的重要作用。与受体相互作用的丝氨酸/苏氨酸蛋白激酶1(RIPK1)已成为坏死过程中的核心角色,它同时调节细胞死亡和炎症反应。本综述深入探讨了 RIPK1 在艾滋病病毒感染期间协调 CD4+ T 细胞坏死的复杂机制。我们探讨了 RIPK1 错综复杂的结构、它与其他信号分子的相互作用以及最终导致细胞坏死的下游事件。此外,我们还讨论了针对 RIPK1 的治疗潜力,以减轻 CD4+ T 细胞的损失并控制 HIV 疾病的发展。了解 RIPK1 在 HIV 诱导的坏死中的多方面作用可能会为新型治疗干预铺平道路,从而对抗这种毁灭性疾病。
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The Role of Receptor-Interacting Serine/Threonine-Protein Kinase 1 (RIPK1) in CD4+ T Cell Necroptosis in HIV Patients: A Narrative Literature Review
The human immunodeficiency virus (HIV) remains a global health challenge, with its ability to deplete CD4+ T cells, leading to acquired immunodeficiency syndrome (AIDS). While apoptosis has been extensively studied in CD4+ T cell depletion, recent research has highlighted the significant role of necroptosis, a regulated form of necrosis, in this process. Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) has emerged as a central player in necroptosis, regulating both cell death and inflammatory responses. This review delves into the intricate mechanisms by which RIPK1 orchestrates necroptosis in CD4+ T cells during HIV infection. We explore the structural intricacies of RIPK1, its interactions with other signaling molecules, and the downstream events that culminate in necroptotic cell death. Additionally, we discuss the therapeutic potential of targeting RIPK1 to mitigate CD4+ T cell loss and control HIV disease progression. Understanding the multifaceted role of RIPK1 in HIV-induced necroptosis may pave the way for novel therapeutic interventions to combat this devastating disease.
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