ReviewCurrent atherosclerosis reports2026
From Inflammation to Targeted Therapy: Leveraging Neutrophil, Platelet, RBC, and Macrophage Biology for Nanocarrier in Atherosclerosis.
Review in Current atherosclerosis reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Targeting Golgi-STING Signaling to Reprogram Innate and Adaptive Immunity for the Treatment of Implant-Associated Infections.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Guided immunotherapy for residual solid tumor: integrating platelets and CAR T cells to reduce post-surgical recurrence.Biomarker research · 2026Review
- Spatial architecture of atherosclerotic plaques: coordinating immune responses through mechanotransduction and vesicular trafficking.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewCell hitchhiking harnesses endogenous circulating cells as programmable carriers to achieve precise, lesion-targeted nanotherapeutic delivery in atherosclerosis. This review examines the mechanistic basis and translational strategies of neutrophil-, platelet-, macrophage-, and red blood cell–based systems, emphasizing their potential to convert the plaque microenvironment from a therapeutic barrier into a receptive target. RECENT
findingsHitchhiking modalities—including surface anchoring, internalization, and membrane cloaking—exploit innate trafficking cues and pathophysiologic triggers such as oxidative stress, matrix metalloproteases, acidic pH, and shear stress to achieve site-specific payload release. Preclinical studies in ApoE⁻/⁻ and large-animal models demonstrate enhanced plaque accumulation, reduced lipid burden, and improved stability using neutrophil-ferried ROS scavengers, platelet-mimetic rapamycin carriers, and macrophage-anchored lipid modulators. These biohybrid platforms benefit from prolonged circulation via CD47-mediated immune evasion and are compatible with PET/MRI theranostics. Hitchhiking strategies address the limitations of conventional nanotherapies by combining active targeting, prolonged bioavailability, and localized release, yet translation faces challenges including off-target immune activation, thrombogenicity, donor variability, and manufacturing hurdles. Standardized preclinical comparisons, rigorous hemocompatibility testing, imaging-guided trials, and hybrid dual-responsive carriers may optimize efficacy and safety. By integrating cellular biology with nanomaterial engineering and regulatory considerations, cell hitchhiking represents a precision approach for durable plaque stabilization and reduced cardiovascular risk.
Indexed as
Identifiers
41733760What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.