Tanveer A. Tabish PhD , Mark J. Crabtree PhD , Helen E. Townley PhD , Paul G. Winyard PhD , Craig A. Lygate PhD
{"title":"Nitric Oxide Releasing Nanomaterials for Cardiovascular Applications","authors":"Tanveer A. Tabish PhD , Mark J. Crabtree PhD , Helen E. Townley PhD , Paul G. Winyard PhD , Craig A. Lygate PhD","doi":"10.1016/j.jacbts.2023.07.017","DOIUrl":null,"url":null,"abstract":"<div><p>A central paradigm of cardiovascular homeostasis is that impaired nitric oxide (NO) bioavailability results in a wide array of cardiovascular dysfunction including incompetent endothelium-dependent vasodilatation, thrombosis, vascular inflammation, and proliferation of the intima. Over the course of more than a century, NO donating formulations such as organic nitrates and nitrites have remained a cornerstone of treatment for patients with cardiovascular diseases. These donors primarily produce NO in the circulation and are not targeted to specific (sub)cellular sites of action. However, safe, and therapeutic levels of NO require delivery of the right amount to a precise location at the right time. To achieve these aims, several recent strategies aimed at therapeutically generating or releasing NO in living systems have shown that polymeric and inorganic (silica, gold) nanoparticles and nanoscale metal-organic frameworks could either generate NO endogenously by the catalytic decomposition of endogenous NO substrates or can store and release therapeutically relevant amounts of NO gas. NO-releasing nanomaterials have been developed for vascular implants (such as stents and grafts) to target atherosclerosis, hypertension, myocardial ischemia-reperfusion injury, and cardiac tissue engineering. In this review, we discuss the advances in design and development of novel NO-releasing nanomaterials for cardiovascular therapeutics and critically examine the therapeutic potential of these nanoplatforms to modulate cellular metabolism, to regulate vascular tone, inhibit platelet aggregation, and limit proliferation of vascular smooth muscle with minimal toxic effects.</p></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"9 5","pages":"Pages 691-709"},"PeriodicalIF":8.4000,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X23003315/pdfft?md5=dc3b7845445ec62e5e749327ff2dddd6&pid=1-s2.0-S2452302X23003315-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"JACC: Basic to Translational Science","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2452302X23003315","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
Abstract
A central paradigm of cardiovascular homeostasis is that impaired nitric oxide (NO) bioavailability results in a wide array of cardiovascular dysfunction including incompetent endothelium-dependent vasodilatation, thrombosis, vascular inflammation, and proliferation of the intima. Over the course of more than a century, NO donating formulations such as organic nitrates and nitrites have remained a cornerstone of treatment for patients with cardiovascular diseases. These donors primarily produce NO in the circulation and are not targeted to specific (sub)cellular sites of action. However, safe, and therapeutic levels of NO require delivery of the right amount to a precise location at the right time. To achieve these aims, several recent strategies aimed at therapeutically generating or releasing NO in living systems have shown that polymeric and inorganic (silica, gold) nanoparticles and nanoscale metal-organic frameworks could either generate NO endogenously by the catalytic decomposition of endogenous NO substrates or can store and release therapeutically relevant amounts of NO gas. NO-releasing nanomaterials have been developed for vascular implants (such as stents and grafts) to target atherosclerosis, hypertension, myocardial ischemia-reperfusion injury, and cardiac tissue engineering. In this review, we discuss the advances in design and development of novel NO-releasing nanomaterials for cardiovascular therapeutics and critically examine the therapeutic potential of these nanoplatforms to modulate cellular metabolism, to regulate vascular tone, inhibit platelet aggregation, and limit proliferation of vascular smooth muscle with minimal toxic effects.
心血管稳态的一个核心范式是,一氧化氮(NO)生物利用率受损会导致一系列心血管功能障碍,包括内皮依赖性血管舒张功能障碍、血栓形成、血管炎症和内膜增生。一个多世纪以来,有机硝酸盐和亚硝酸盐等 NO 供体制剂一直是治疗心血管疾病患者的基石。这些供体主要在血液循环中产生 NO,并不针对特定的(亚)细胞作用位点。然而,要使 NO 达到安全和治疗水平,就必须在正确的时间向正确的部位输送正确的剂量。为了实现这些目标,最近几种旨在治疗性地在活体系统中产生或释放 NO 的策略表明,聚合物和无机(硅、金)纳米粒子以及纳米级金属有机框架可以通过催化分解内源性 NO 底物产生内源性 NO,或者可以储存和释放治疗相关量的 NO 气体。针对动脉粥样硬化、高血压、心肌缺血再灌注损伤和心脏组织工程的血管植入物(如支架和移植物)已开发出释放 NO 的纳米材料。在这篇综述中,我们将讨论用于心血管治疗的新型 NO 释放纳米材料的设计和开发进展,并认真研究这些纳米平台在调节细胞代谢、调节血管张力、抑制血小板聚集和限制血管平滑肌增殖方面的治疗潜力,同时将其毒性效应降至最低。
期刊介绍:
JACC: Basic to Translational Science is an open access journal that is part of the renowned Journal of the American College of Cardiology (JACC). It focuses on advancing the field of Translational Cardiovascular Medicine and aims to accelerate the translation of new scientific discoveries into therapies that improve outcomes for patients with or at risk for Cardiovascular Disease. The journal covers thematic areas such as pre-clinical research, clinical trials, personalized medicine, novel drugs, devices, and biologics, proteomics, genomics, and metabolomics, as well as early phase clinical trial methodology.