Atherosclerosis is the leading cause of cardiovascular disease and myocardial infarction. Precise and effective plaque targeting is a major objective for therapeutic outcomes throughout various stages of atherosclerosis. Inspired by the natural recruitment of neutrophils in atherosclerotic plaques, we fabricated a simvastatin (ST)-loaded and neutrophil membrane-cloaked nanoplatform (NNP) for enhancing localized payload delivery and atherosclerosis management. The resulting NNP mimicked neutrophil function and significantly decreased macrophage-mediated phagocytosis to prolong its own circulation time in the blood. Compared to pristine nanoparticles (NP) without a membrane coating, NNP achieved better plaque targeting in ApoE mice, as indicated by neutrophils actively recruited in atherosclerotic lesions. The higher plaque homing with NNP was monitored by dynamic fluorescence/magnetic resonance (MR) dual-modality imaging. The results further showed that NNP efficiently prevented atherosclerosis development mainly by suppressing local inflammatory macrophages, and the percentage of plaques in the entire aortic area was reduced to 4.75 ± 1.48 % following NNP treatment. A biosafety assessment indicated that the biomimetic NNP induced no noticeable toxicity in the body. This approach of neutrophil membrane-camouflaged nanoparticles offers new opportunities to various therapeutic agents for on-demand delivery in neutrophil-involved inflammatory diseases.
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http://dx.doi.org/10.1016/j.mtbio.2024.101397 | DOI Listing |
Mater Today Bio
February 2025
Department of Radiology and Tianjin Key Laboratory of Functional Imaging, Tianjin Medical University General Hospital, Tianjin, 300052, PR China.
Atherosclerosis is the leading cause of cardiovascular disease and myocardial infarction. Precise and effective plaque targeting is a major objective for therapeutic outcomes throughout various stages of atherosclerosis. Inspired by the natural recruitment of neutrophils in atherosclerotic plaques, we fabricated a simvastatin (ST)-loaded and neutrophil membrane-cloaked nanoplatform (NNP) for enhancing localized payload delivery and atherosclerosis management.
View Article and Find Full Text PDFAtherosclerosis, a slowly progressing inflammatory disease, is characterized by the presence of monocyte-derived macrophages. Interventions targeting the inflammatory characteristics of atherosclerosis hold promising potential. Although interleukin (IL)-10 is widely acknowledged for its anti-inflammatory effects, systemic administration of IL-10 has limitations due to its short half-life and significant systemic side effects.
View Article and Find Full Text PDFFolia Histochem Cytobiol
January 2025
Department of Clinical Laboratory, Guangzhou Twelfth People's Hospital, Guangzhou, China.
Introduction: . Pyroptosis is closely related to many chronic diseases including atherosclerosis, but the potential pathomechanisms are still unclear. This research aimed to explore how lncRNAs may contribute to pyroptosis and the potential mechanisms.
View Article and Find Full Text PDFJ Prev Alzheimers Dis
January 2025
School of Health and Biomedical Sciences, RMIT University, 220 3-5 Plenty Road, Bundoora VIC 3082, Australia. Electronic address:
Alzheimer's Disease (AD) is a chronic neurodegenerative disorder characterized by the accumulation of toxic amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) of tau protein in the brain. Microglia, key immune cells of the central nervous system, play an important role in AD development and progression, primarily through their responses to Aβ and NFTs. Initially, microglia can clear Aβ, but in AD, chronic activation overwhelms protective mechanisms, leading to sustained neuroinflammation that enhances plaque toxicity, setting off a damaging cycle that affects neurons, astrocytes, cerebral vasculature, and other microglia.
View Article and Find Full Text PDFJ Prev Alzheimers Dis
January 2025
CenExel iResearch, Atlanta, GA, USA.
Background: Soluble species of multimeric amyloid-beta including globular amyloid-beta oligomers (AβOs) and linear amyloid-beta protofibrils are toxic to neurons. Sabirnetug (ACU193) is a humanized monoclonal antibody, raised against globular species of soluble AβO, that has over 650-fold greater binding affinity for AβOs over monomers and appears to have relatively little binding to amyloid plaque.
Objectives: To assess safety, pharmacokinetics, and exploratory measures including target engagement, biomarker effects, and clinical efficacy of sabirnetug in participants with early symptomatic Alzheimer's disease (AD; defined as mild cognitive impairment and mild dementia due to AD).
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