Exploiting passive nanomedicine accumulation at sites of enhanced vascular permeability for non-cancerous applications

Durymanov, Mikhail; Kamaletdinova, Tatiana; Lehmann, Sarah E.; Reineke, Joshua

doi:10.1016/j.jconrel.2017.06.013

Cited by 70 publications

(53 citation statements)

References 179 publications

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“…Moreover, in vivo we found evidence via immunofluorescence of macrophages with CD11b staining of association of both CDDO-Me-NPs and LDL-OA-NPs with atherosclerotic plaque macrophages. Their accumulation is consistent with the literature which shows that NPs can also accumulate selectively in atherosclerotic plaque simply due to the enhanced permeation and retention (EPR) effect [42][43] . NPs take advantage of a dysfunctional endothelium with larger inter-endothelial junctions to accumulate in sites of vascular inflammation [42][43] .…”

Section: Cddo-me-npssupporting

confidence: 92%

“…Their accumulation is consistent with the literature which shows that NPs can also accumulate selectively in atherosclerotic plaque simply due to the enhanced permeation and retention (EPR) effect [42][43] . NPs take advantage of a dysfunctional endothelium with larger inter-endothelial junctions to accumulate in sites of vascular inflammation [42][43] . Early atherosclerotic events have been shown to be associated with more severe endothelial barrier disruption, whilst advanced stage disease progressions are associated with improved endothelial barrier permeability 42 .…”

Section: Cddo-me-npssupporting

confidence: 92%

“…Early atherosclerotic events have been shown to be associated with more severe endothelial barrier disruption, whilst advanced stage disease progressions are associated with improved endothelial barrier permeability 42 . Previous pre-clinical studies have successfully integrated NPs into sites of atherosclerotic plaque, some of which were able to inhibit plaque formation and decreased the number of atherosclerotic lesions in mouse models of atherosclerosis 39,[43][44][45][46][47] . Macrophage-mediated uptake of NPs in vivo is also likely to reflect phagocytosis due to the presence of the NP-protein corona that plays a role in NP-cell interactions 48 .…”

Section: Cddo-me-npsmentioning

confidence: 99%

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Nrf2 activator-encapsulating polymeric nanoparticles and LDL-like nanoparticles target atherosclerotic plaque

Maiocchi

Thai

Buglak

et al. 2020

Preprint

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Atherosclerotic vascular disease is the leading cause of death world-wide with few novel therapies available in spite of the ongoing health burden. Oxidative stress is a wellestablished driver of atherosclerotic progression; however the clinical translation of redoxbased therapies is lacking. One of the challenges facing redox-based therapies is their targeted delivery to cellular domains of redox dysregulation. In the current study we sought to develop NPs encapsulating redox-based interventions that exploit passive means of targeting to selectively accumulate in atherosclerotic plaque with the aim of enhancing the intra-plaque bioavailability of interventions. Herein we present two types of nanoparticles (NPs): (i) We have employed flash nanoprecipitation to synthesize polymeric NPs encapsulating the hydrophobic Nrf2 activator drug, CDDO-Methyl, (ii) we have generated LDL-like NPs encapsulating the anti-inflammatory compound, oleic acid (OA). Nrf2activators are a promising class of redox-active drug molecules whereby activation of Nrf2 results in the expression of several antioxidant and cyto-protective enzymes. Moreover, local activation of Nrf2 within the atherosclerotic plaque can be athero-protective. In this study we characterize the physiochemical properties of these NPs as well as confirm in vitro association of NPs with murine macrophages. In vitro drug release of CDDO-Me from polymeric NPs was determined by Nrf2-ARE-driven GFP fluorescence. In vivo localization was assessed through immunofluorescence of histological sections. We show that CDDO-Me-NPs and LDL-OA-NPs selectively accumulate in atherosclerotic plaque of two widelyused murine models of atherosclerosis: ApoE -/and LDLr -/mice. Overall, these studies underline that passive targeting of atherosclerotic plaque is an effective means to enhance delivery of redox-based interventions. Future work will assess the therapeutic efficacy of intra-plaque Nrf2 activation or anti-inflammatory actions with CDDO-

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Section: Cddo-me-npssupporting

confidence: 92%

Section: Cddo-me-npssupporting

confidence: 92%

Section: Cddo-me-npsmentioning

confidence: 99%

See 1 more Smart Citation

Nrf2 activator-encapsulating polymeric nanoparticles and LDL-like nanoparticles target atherosclerotic plaque

Maiocchi

Thai

Buglak

et al. 2020

Preprint

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“…With the progression of inflammation, the blood‐joint barrier is disrupted, resulting leaky blood vasculature system in joints. Therefore, NMs largely enable the availability of medicaments at the diseased articular sites with heightened accumulation via EPR‐like effect and thus attenuate the adverse effects on normal tissues …”

Section: Targeting Nms Relieve the Att Of Ramentioning

confidence: 99%

“…Therefore, NMs largely enable the availability of medicaments at the diseased articular sites with heightened accumulation via EPR-like effect and thus attenuate the adverse effects on normal tissues. [27] Existing studies have indicated superior therapeutic effects of NMs with appropriate sizes and surface chemical nature. It has been demonstrated that NMs bigger than 200 nm can be eliminated by spleen and NMs with a size smaller than 10 nm can pass through kidney's filtration system.…”

Section: Nms Overcome Att Of Ra Via Passive Targeting Strategiesmentioning

confidence: 99%

Move to Nano‐Arthrology: Targeted Stimuli‐Responsive Nanomedicines Combat Adaptive Treatment Tolerance (ATT) of Rheumatoid Arthritis

Liu

Guo

Liang

2018

Biotechnology Journal

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Rheumatoid arthritis (RA) is one of the most popular chronic autoimmune diseases characterized with persistent synovial inflammation and bone destruction. Although considerable developments have been gained in clinical treatment of RA, the major drawback to RA therapy stems from the adaptive treatment tolerance (ATT) following the long-term drug use, which causes compromised efficacy, sustained drug dose increase, and severe adverse events. To address these challenges, it is of great significance to put forward innovative therapeutic approaches for RA treatment. Nowadays, developments of nanotechnology-based nanomedicines (NMs) for RA are in progress. Multifunctional NMs with targeted stimuli-responsive features have been one of the central concepts in designing more accessible formulations for efficient RA treatment. These NMs are able to postpone RA progression effectively, because of their delivery and on-demand release of medicaments at targeted sites in response to external or internal stimuli related to the RA pathophysiology without obvious adverse side-effects on the normal tissues. Therefore, NMs have gained interest from pre-clinical research scientists as well as clinical doctors worldwide. Herein, the authors highlight the recent attempts of targeted stimuli-responsive NMs for RA therapy in the last 5 years. The described progresses may pave the way to novel and highly effective RA NMs.

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SupramolecularPeptide‐basedNanomaterials for the Treatment of Fibrosis

Liu,

Zou

2024

Peptide Self‐Assembly and Engineering

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Exploiting passive nanomedicine accumulation at sites of enhanced vascular permeability for non-cancerous applications

Cited by 70 publications

References 179 publications

Nrf2 activator-encapsulating polymeric nanoparticles and LDL-like nanoparticles target atherosclerotic plaque

Nrf2 activator-encapsulating polymeric nanoparticles and LDL-like nanoparticles target atherosclerotic plaque

Move to Nano‐Arthrology: Targeted Stimuli‐Responsive Nanomedicines Combat Adaptive Treatment Tolerance (ATT) of Rheumatoid Arthritis

SupramolecularPeptide‐basedNanomaterials for the Treatment of Fibrosis

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