更新于：2024-11-01

P2Y1

更新于：2024-11-01

基本信息

别名

ADP receptor、P2RY1、P2Y purinoceptor 1

+ [6]

简介

Receptor for extracellular adenine nucleotides such as ADP (PubMed:9442040, PubMed:9038354, PubMed:25822790). In platelets, binding to ADP leads to mobilization of intracellular calcium ions via activation of phospholipase C, a change in platelet shape, and ultimately platelet aggregation (PubMed:9442040).

关联

项与 P2Y1 相关的药物

P2Y1 Antagonist(Bristol Myers Squibb)

靶点

P2Y1

作用机制

P2Y1拮抗剂

在研机构

Bristol Myers Squibb Co.

原研机构

Bristol Myers Squibb Co.

在研适应症

血栓形成

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

MRS 2603

靶点

P2Y1 x P2Y13 receptor

作用机制

P2Y1拮抗剂 [+1]

在研机构

Gwangju Institute of Science & Technology

原研机构

Gwangju Institute of Science & Technology

在研适应症-

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

BMS-884775

靶点

P2Y1

作用机制

P2Y1拮抗剂

在研机构

Bristol Myers Squibb Co.

原研机构

Bristol Myers Squibb Co.

在研适应症

血栓形成

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 P2Y1 相关的临床结果

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100 项与 P2Y1 相关的转化医学

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0 项与 P2Y1 相关的专利（医药）

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1,179

项与 P2Y1 相关的文献（医药）

2025-02-01·Neural Regeneration Research

P2Y1 receptor in Alzheimer’s disease

Article

作者: Luo, Shan ; Wang, Yifei ; Hisatsune, Tatsuhiro

Alzheimer’s disease is the most frequent form of dementia characterized by the deposition of amyloid-beta plaques and neurofibrillary tangles consisting of hyperphosphorylated tau. Targeting amyloid-beta plaques has been a primary direction for developing Alzheimer’s disease treatments in the last decades. However, existing drugs targeting amyloid-beta plaques have not fully yielded the expected results in the clinic, necessitating the exploration of alternative therapeutic strategies. Increasing evidence unravels that astrocyte morphology and function alter in the brain of Alzheimer’s disease patients, with dysregulated astrocytic purinergic receptors, particularly the P2Y1 receptor, all of which constitute the pathophysiology of Alzheimer’s disease. These receptors are not only crucial for maintaining normal astrocyte function but are also highly implicated in neuroinflammation in Alzheimer’s disease. This review delves into recent insights into the association between P2Y1 receptor and Alzheimer’s disease to underscore the potential neuroprotective role of P2Y1 receptor in Alzheimer’s disease by mitigating neuroinflammation, thus offering promising avenues for developing drugs for Alzheimer’s disease and potentially contributing to the development of more effective treatments.

2024-11-01·Journal of Neurochemistry

Astrocytic purinergic signalling contributes to the development and maintenance of neuropathic pain via modulation of glutamate release

Article

作者: Liu, Suting ; Ji, Qing ; Tang, Jun ; Zhu, Chao ; Cui, Liying ; Li, Yunzi ; Jin, Li ; Cheng, Hao

AbstractAlthough activation of astrocytes is critical in developing neuropathic pain (NP) following nerve injury, the underlying mechanisms of NP and therapeutic management for NP are still vague. Importantly, the decreases in the levels of astrocytic glutamate transporter‐1 (GLT‐1) in the spinal dorsal horn result in enhanced excitatory transmission and cause persistent pain. P2Y1 purinergic receptor (P2Y1R) has been shown to enhance many inflammatory processes. The up‐regulated expression of astrocytic P2Y1R is crucial to participate in pain transduction under conditions of nerve injury and peripheral inflammation considering that P2Y1R is potentially involved in glutamate release and synaptic transmission. This study indicates that the expression of P2Y1R in the spinal cord was increased accompanied by the activation of A1 phenotype astrocytes in the rat model of spinal nerve ligation (SNL). Astrocyte‐specific knockdown of P2Y1R alleviated SNL‐induced nociceptive responses and mitigated A1 reactive astrocytes, which subsequently increased GLT‐1 expression. Conversely, in naïve rats, P2Y1R over‐expression induced a canonical NP‐like phenotype and spontaneous hypernociceptive responses and increased the concentration of glutamate in the spinal dorsal horn. Besides, our in vitro data showed that the proinflammatory cytokine tumour necrosis factor‐alpha contributes to A1/A2 astrocyte reactivity and Ca2+‐dependent release of glutamate. Conclusively, our results provide novel insights that as a significant regulator of astrocytic A1/A2 polarization and neuroinflammation, P2Y1R may represent a potential target for the treatment of SNL‐induced NP.

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2024-09-01·The American Surgeon™

The Impact of ADP Inhibition on Traumatic Brain Injury Outcomes

Article

作者: Briggs, Steven ; Howe, Chase ; Cao, Li ; Mathies, Amanda ; Sang, Tyler ; Nielsen, Dana

Platelet inhibition correlates with severity of traumatic brain injury and may be associated with mortality. Adenosine diphosphate participates in platelet aggregation via the activation of the ADP receptors, P2Y1 and P2Y12. Prior work suggests this ADP pathway is significant in managing patients with head injuries. This study aimed to measure the influence of ADP inhibition on outcomes after a traumatic brain injury (TBI), as measured by thromboelastography with platelet mapping (TEG-PM). Outcomes were defined as (a) hospital length of stay; (b) ICU length of stay, (c) mortality, and (d) progression of hemorrhage on CT. The resulting cohort was split into quartiles to compare the effect of increasingly inhibited ADP values on the identified outcomes. Comparisons of 2 groups of patients were also conducted, one defined by ADP inhibition less than or equal to 60% and the other group by ADP inhibition of greater than 60%. 98 patients were included in final analysis, with 72.4% having ADP inhibition less than 60%. These patients were significantly older and had lower global injury severity scores (ISSs), although their head-specific ISS was equivalent. Compared to the group with ADP inhibition over 60%, there was no significant difference in mortality, hospital or ICU length of stay, or progression of lesion on CT. Patients with ADP less than 60% inhibited had smaller ISS and higher GCS, indicating they were less injured than those with greater ADP inhibition, consistent with prior literature. The equivalent ICU and hospital length of stay and mortality suggests that ADP inhibition plays a smaller role in outcomes. Additional study with a larger sample size and guideline-based assessments is necessary to further define the impact of ADP inhibition and to determine the role of platelet transfusion in this population.