Targeting Atherosclerosis via NEDD4L Signaling-A Review of the Current Literature.

IF 3.6 3区 生物学 Q1 BIOLOGY
Lucas Fornari Laurindo, Victória Dogani Rodrigues, Enzo Pereira de Lima, Beatriz Leme Boaro, Julia Maria Mendes Peloi, Raquel Cristina Ferraroni Sanches, Cláudia Rucco Penteado Detregiachi, Ricardo José Tofano, Maria Angelica Miglino, Katia Portero Sloan, Lance Alan Sloan, Sandra Maria Barbalho
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引用次数: 0

Abstract

Cardiovascular diseases are the primary cause of mortality worldwide. In this scenario, atherosclerotic cardiovascular outcomes dominate since their incidence increases as populations grow and age. Atherosclerosis is a chronic inflammatory disease that affects arteries. Although its pathophysiology is heterogeneous, some genes are indissociably associated with its occurrence, and understanding their effects on the disease's occurrence could undoubtedly define effective screening and treatment strategies. One such gene is NEDD4L. The NEDD4L gene is related to ubiquitin ligase enzyme activities. It is essential to regulate vascular inflammation, atherosclerosis plaque stability, endothelial and vascular smooth cell function, and lipid metabolism, particularly in controlling cholesterol levels. However, the evidence is dubious, and no review has yet synthesized the effects of targeting NEDD4L on atherosclerosis. Therefore, our review aims to fill this gap by analyzing the literature on NEDD4L concerning atherosclerosis occurrence. To achieve this goal, we performed a systematic literature search of reputable databases, including PubMed, Google Scholar, Web of Science, Scopus, and Embase. The inclusion criteria comprised peer-reviewed original studies using in vitro and animal models due to the unavailability of relevant clinical studies. Systematic reviews, meta-analyses, and articles that did not focus on the relationship between NEDD4L and atherosclerosis and those unrelated to this health condition were excluded. Studies not written in the English language were also excluded. The search strategy included studies from January 2000 to January 2025 in the final analysis to capture recent advancements. Following screening, five studies were included. Most of the included studies underscored NEDD4L's role in increasing atherosclerosis plaque formation, but other studies indicated that stimulating NEDD4L may positively counter atherosclerosis plaque formation. Therefore, future research endeavors must address several limitations, which have been tentatively highlighted throughout the manuscript, for more informative research based on preclinical studies and to successfully translate the findings into clinical trials.

通过NEDD4L信号靶向动脉粥样硬化——当前文献综述
心血管疾病是全世界死亡的主要原因。在这种情况下,动脉粥样硬化性心血管结果占主导地位,因为其发病率随着人口增长和年龄增长而增加。动脉粥样硬化是一种影响动脉的慢性炎症性疾病。虽然其病理生理是异质的,但一些基因与其发生有着不可分离的联系,了解它们对疾病发生的影响无疑可以确定有效的筛查和治疗策略。其中一个基因是NEDD4L。NEDD4L基因与泛素连接酶活性有关。它对调节血管炎症、动脉粥样硬化斑块稳定性、内皮细胞和血管平滑细胞功能以及脂质代谢,特别是控制胆固醇水平至关重要。然而,证据是可疑的,目前还没有综述综合了靶向NEDD4L对动脉粥样硬化的影响。因此,我们的综述旨在通过分析NEDD4L与动脉粥样硬化发生的文献来填补这一空白。为了实现这一目标,我们对知名数据库进行了系统的文献检索,包括PubMed、谷歌Scholar、Web of Science、Scopus和Embase。由于缺乏相关临床研究,纳入标准包括使用体外和动物模型的同行评议原始研究。系统评价、荟萃分析和没有关注NEDD4L与动脉粥样硬化之间关系的文章被排除在外。非英语研究也被排除在外。搜索策略包括从2000年1月到2025年1月的研究,最终分析了最近的进展。筛选后,纳入了5项研究。大多数纳入的研究强调了NEDD4L在增加动脉粥样硬化斑块形成中的作用,但其他研究表明,刺激NEDD4L可能积极对抗动脉粥样硬化斑块的形成。因此,未来的研究努力必须解决几个限制,这些限制在整个手稿中都暂时强调了,以便在临床前研究的基础上进行更多的信息研究,并成功地将研究结果转化为临床试验。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Biology-Basel
Biology-Basel Biological Science-Biological Science
CiteScore
5.70
自引率
4.80%
发文量
1618
审稿时长
11 weeks
期刊介绍: Biology (ISSN 2079-7737) is an international, peer-reviewed, quick-refereeing open access journal of Biological Science published by MDPI online. It publishes reviews, research papers and communications in all areas of biology and at the interface of related disciplines. Our aim is to encourage scientists to publish their experimental and theoretical results in as much detail as possible. There is no restriction on the length of the papers. The full experimental details must be provided so that the results can be reproduced. Electronic files regarding the full details of the experimental procedure, if unable to be published in a normal way, can be deposited as supplementary material.
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