Table 2.
Selected reviews.
| Review focus | Covered topics | Covered period | Study models treated | Remarks | References |
|---|---|---|---|---|---|
| Nanoparticle mediated detection and treatment of AS; prevention of plaque progression. | Atherogenesis, NPs for structural/functional imaging and therapy, preclinical stages, anti-inflammation and lipid lowering strategies, targeting routes. | Mainly 2000–2015, back to 1993. | In vitro, in vivo, pre-clinical stage. | NPs efficiency in the field is plenty documented in vitro and in vivo only, preclinical and clinical studies still fall behind. Useful tables summarizing researches done on detection and treatment of atherosclerosis using nanoparticles. |
Zhang et al., 2017 |
| Immune cells in healthy and AS-prone aorta. | (Sub)phenotypes classification of dendritic cells and MΦs possibly present in aortic walls, their roles in AS; mixed phenotypes | Mainly 2004–2011, back to 1913. | In vitro, in vivo. | Useful table of ICs classification, markers, secreted factors, functions, impact on plaque stability. | Butcher and Galkina, 2012 |
| Lipids in cardiovascular systems | Metabolism and blood transport of cholesterols, triglycerides and other lipids. | 1973–2017, one from 1954. | In vitro, in vivo, clinical. | Focus on the role of triglycerides, but contains a short and efficient discussion on cholesterol metabolism and transport, interaction with MΦs and role in AS. | |
| NPs as drug delivery systems for cardiovascular disorder. | NPs performances on drug kinetics and toxicity, various nanoconstructs design/synthesis and their physiological behavior, AS, most fundamental MCs and MΦs types in humans and mice. | Mainly 2005–2016, back to 1994. | In vitro, in vivo, pre-clinical stage. | Short review. | Matoba et al., 2017 |
| Vascular targeting of NPs for molecular imaging of diseased endothelium. | Rational design of physicochemical NPs properties, AS, cancer, disease-impaired blood flows. Imaging modalities (nuclear, optical, computed, tomography, magnetic resonance, ultrasound, multimodal) for NPs. |
Mainly 2006–2016, back to 1981. | In vitro, in vivo, pre-clinical stage. | Imaging should be pondered to achieve complex information, not just images. No significant discrepancies in clinical translation of results from animal models of the disease. Authors feel a lack in clear clinical relevance or of a well-defined endpoint; this leads to poorly designed preclinical studies. However, also early-stage researches in the field are starting to consider clinical deployments. |
Atukorale et al., 2017 |
| Rational design of NPs for AS. | Early and late stage of the disease, NPs/cell interaction, biodistribution, drug delivery, multi-modal imaging, AS-oriented gene therapies. | Mainly 2008–2016, back to 1958. | In vitro, in vivo, pre-clinical stage. | Useful table with a summary of nanomaterials designed to image or modulate atherosclerotic lesions. | Allen et al., 2016 |
| Taking advance of the immune system cells for therapeutic purposes. | NPs fate upon injection, physicochemical properties for rational design, cellular uptake mechanism, passive and active targeting. MΦs subtypes, markers, produced cytokines, polarization control; imaging of inflammation. | Mainly 2003–2015, back to 1977. | In vitro, in vivo, clinical. | NPs targeting MΦs and controlling their polarization are just beginning to be elaborated by the community and probably their potential are not yet grasped. Authors suggest the implementation of MΦs specificity in theranostic nano-constructs constitutes a strategic step to expedite transition into clinical phase. | Pentecost et al., 2016 |
| Nanoliposomes and NPs toward cardiovascular related disorders. | Principles of action, drug release and interaction, infarcted heart, lesions imaging modalities. | Mainly 2005–2016, back to 1998. | In vitro, in vivo, clinical. | Nanoliposomal formulations are promising vectors for cardiovascular disorders diagnosis and treatment, but side effects should be reduced bioactives controlled release optimized, also for fastening clinical translation. | Cheraghi et al., 2017 |
| Mouse models for AS. | Disease development and plaque rupture, pro and cons of most common mouse models, endoplasmic reticulum stress, mitochondrial dysfunction. | Mainly 2004–2016, back to 1977. | In vivo, clinical. | The complexity of the topic does not allow for a single, good-for-all animal model. Importantly, a correct study design must go through the identification and comprehension of the molecular events involved. | Lee et al., 2017 |
| Animal models for AS. | Mice models for AS and for plaque rupture, rabbit models, pigs, non-human primates. | Mainly 2000–2016, back to 1980. | In vivo. | One discriminant among different animal models for AS plaques is the topography of the generated lesions, compared to humans. In this scenario mice became the predominant species for models related to inflammatory cardiovascular diseases. Rabbits fall just behind and are mainly exploited due to their plasma metabolism similarity with humans. ApoE−/−Fbn1C1039G+/− mice hold high promises for the future, being the very first animal model presenting spontaneous plaque rupture with end-points similar to humans. | Emini Veseli et al., 2017 |
AS, atherosclerosis; IC, immune cell; MC, monocyte; MΦ, macrophage; NP, nanoparticle; ApoE, apolipoprotein E.