Fluorescent probes capable of precise detection of atherosclerosis (AS) at an early stage and fast assessment of anti‐AS drugs in animal level are particularly valuable. Herein, a highly bright aggregation‐induced emission (AIE) nanoprobe is introduced by regulating the substituent of rhodanine for early detection of atherosclerotic plaque and screening of anti‐AS drugs in a precise, sensitive, and rapid manner. With dicyanomethylene‐substituted rhodanine as the electron‐withdrawing unit, the AIE luminogen named TPE‐T‐RCN shows the highest molar extinction coefficient, the largest photoluminescence quantum yield, and the most redshifted absorption/emission spectra simultaneously as compared to the control compounds. The nanoprobes are obtained with an amphiphilic copolymer as the matrix encapsulating TPE‐T‐RCN molecules, which are further surface functionalized with anti‐CD47 antibody for specifically binding to CD47 overexpressed in AS plaques. Such nanoprobes allow efficient recognition of AS plaques at different stages in apolipoprotein E‐deficient (apoE−/−) mice, especially for the recognition of early‐stage AS plaques prior to micro‐computed tomography (CT) and magnetic resonance imaging (MRI). These features impel to apply the nanoprobes in monitoring the therapeutic effects of anti‐AS drugs, providing a powerful tool for anti‐AS drug screening. Their potential use in targeted imaging of human carotid plaque is further demonstrated.
Percutaneous coronary intervention for coronary artery disease treatment often results in pathological vascular injury, characterized by P‐selectin overexpression. Adipose‐derived stem cells (ADSCs) therapeutic efficacy remains elusive due to poor ADSCs targeting and retention in injured vessels. Here, conjugated P‐selectin binding peptide (PBP) to polyethylene glycol‐conjugated phospholipid derivative (DMPE‐PEG) linkers (DMPE‐PEG‐PBP; DPP) are used to facilitate the modification of PBP onto ADSCs cell surfaces via hydrophobic interactions between DMPE‐PEG and the phospholipid bilayer. DPP modification neither has influence on ADSCs proliferation nor apoptosis/paracrine factor gene expression. A total of 5 × 10−6 m DPP‐modified ADSCs (DPP‐ADSCs) strongly binds to P‐selectin‐displaying activated platelets and endothelial cells (ECs) in vitro and to wire‐injured rat femoral arteries when administered by intra‐arterial injection. Targeted binding of ADSCs shields injury sites from platelet and leukocyte adhesion, thereby decreasing inflammation at injury sites. Furthermore, targeted binding of ADSCs recovers injured ECs functionality and reduces platelet‐initiated vascular smooth muscle cells (VSMCs) chemotactic migration. Targeted binding of DPP‐human ADSCs to balloon‐injured human femoral arteries is also demonstrated in ex vivo experiments. Overall, DPP‐ADSCs promote vascular repair, inhibit neointimal hyperplasia, increase endothelium functionality, and maintain normal VSMCs alignment, supporting preclinical noninvasive utilization of DPP‐ADSCs for vascular injury.
Fine particulate matter ≤2.5 μm (PM2.5) air pollution is regarded as one of the prominent risk factors that contributes to morbidity and mortality globally, among which cardiovascular disease (CVD) has been strongly associated with PM2.5 exposure and is a leading cause of death. Atherosclerosis (AS), the common pathological basis of many CVDs, is a progressive syndrome characterized by the accumulation of lipids and fibrous plaque in the arteries. Recent epidemiological and toxicological studies suggest that PM2.5 may also contribute to the development of AS, even at levels below the current air quality standards. In this paper, the complete pathological process of atherosclerotic plaque from occurrence to rupture leading to CVD was elaborated. Then, the growing epidemiological evidence linking PM2.5 to AS in humans was reviewed and summarized. Furthermore, the potential mechanisms of PM2.5‐mediated AS were discussed, including oxidative stress, inflammation, endothelial dysfunction, abnormal lipid metabolism, disturbance of the autonomic nervous system, and abnormal coagulation function. This paper aimed to provide a comprehensive view of the effect of PM2.5 on the occurrence and development of AS for better prevention and mitigation of adverse health impacts due to PM2.5 air pollution.
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