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Purpose of Review <p>Cell 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.</p> Recent Findings <p>Hitchhiking 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.</p> Summary <p>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.</p>

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From Inflammation to Targeted Therapy: Leveraging Neutrophil, Platelet, RBC, and Macrophage Biology for Nanocarrier in Atherosclerosis

  • 期刊论文

  • 发表日期：

    2026年2月24日

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  • Farshad Heydari,
  • Michael R. Hamblin,
  • Jalal Naghinezhad

摘要

Purpose of Review

Cell 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 Findings

Hitchhiking 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.

Summary

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.