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Cocaine addicted to cytoskeletal change and a fibrosis high.
Cytoskeleton ( IF 2.4 ) Pub Date : 2019-01-22 , DOI: 10.1002/cm.21510
Avnish Verma 1 , Jason Bennett 2 , Ayşe Merve Örme 1 , Elena Polycarpou 1 , Brian Rooney 1
Affiliation  

Cocaine is one of the most widely abused illicit drugs due to its euphoric and addictive properties. Cocaine‐mediated cognitive impairments are the result of dynamic cytoskeletal rearrangements involved in mediating structural and behavioural plasticity. Cytoskeletal changes initiated following cocaine abuse are regulated by the Rho family of GTPases with significant downstream activity in key actin binding proteins. Moreover, signalling via the endoplasmic reticulum chaperone protein, sigma‐1 receptor has highlighted the possibility of cocaine regulated pathology in other organ systems. However, the question of whether upstream stimulation of such a high affinity binding receptor is directly involved in cocaine‐mediated cytoskeletal changes at present remains unknown. In this review, we describe the functional role of key cytoskeletal regulators in response to cocaine‐induced signalling cues. In addition, we ascertain the extent of whether global cytoskeletal modulators involved in cocaine‐induced neurological stimulation can be used as a platform for future studies into elucidating its fibrotic potential within the hepatic microenvironment. A focus on aspects still poorly understood relating to the nonneuronal pathological impact of cocaine is discussed in the sphere of hepatic dysregulation. Lastly, we suggest that cocaine may mediate its pathological capacity via the sigma1 receptor in regulating hepatoxicity, hepatic stellate cells activity, cytoskeletal dynamics, and the transcriptional regulation of key hepato‐fibrogenic modulators.

中文翻译:

可卡因沉迷于细胞骨架变化和高纤维化。

由于可卡因的欣快和成瘾性,它是滥用最广泛的非法药物之一。可卡因介导的认知障碍是动态细胞骨架重排的结果,其参与介导结构和行为可塑性。可卡因滥用后引发的细胞骨架变化受GTPases Rho家族的调节,在关键肌动蛋白结合蛋白中具有显着的下游活性。此外,通过内质网伴侣蛋白sigma-1受体发出的信号突出了可卡因调节其他器官系统病理的可能性。但是,目前尚不清楚这种高亲和力结合受体的上游刺激是否直接参与可卡因介导的细胞骨架变化。在这篇评论中 我们描述了可卡因诱导的信号提示响应中关键细胞骨架调节剂的功能作用。此外,我们确定参与可卡因诱导的神经系统刺激的整体细胞骨架调节剂是否可以用作未来研究的平台,以阐明其在肝微环境中的纤维化潜力。在肝脏失调领域中,讨论了对可卡因的非神经病理性影响仍知之甚少的方面的讨论。最后,我们建议可卡因可能通过sigma1受体介导其病理能力,以调节肝毒性,肝星状细胞活性,细胞骨架动力学以及关键的肝纤维化调节剂的转录调控。我们确定参与可卡因诱导的神经系统刺激的整体细胞骨架调节剂是否可以用作未来研究的平台,以阐明其在肝微环境中的纤维化潜力。在肝脏失调领域中,讨论了对可卡因的非神经病理性影响仍知之甚少的方面的讨论。最后,我们建议可卡因可能通过sigma1受体介导其病理能力,以调节肝毒性,肝星状细胞活性,细胞骨架动力学以及关键的肝纤维化调节剂的转录调控。我们确定参与可卡因诱导的神经系统刺激的整体细胞骨架调节剂是否可以用作未来研究的平台,以阐明其在肝微环境中的纤维化潜力。在肝脏失调领域中,讨论了对可卡因的非神经病理性影响仍知之甚少的方面的讨论。最后,我们建议可卡因可能通过sigma1受体介导其病理能力,以调节肝毒性,肝星状细胞活性,细胞骨架动力学以及关键的肝纤维化调节剂的转录调控。在肝脏失调领域中,讨论了对可卡因的非神经病理性影响仍知之甚少的方面的讨论。最后,我们建议可卡因可能通过sigma1受体介导其病理能力,以调节肝毒性,肝星状细胞活性,细胞骨架动力学以及关键的肝纤维化调节剂的转录调控。在肝脏失调领域中,讨论了对可卡因的非神经病理性影响仍知之甚少的方面的讨论。最后,我们建议可卡因可能通过sigma1受体介导其病理能力,以调节肝毒性,肝星状细胞活性,细胞骨架动力学以及关键的肝纤维化调节剂的转录调控。
更新日期:2019-01-22
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