Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

Decursin-Loaded Nanovesicles Target Macrophages Driven by the Pathological Process of Atherosclerosis

Chen H., Zhang Y., Aikebaier M., Du Y., Liu Y., Zha Q.

Animal Study on Cardiovascular Disease, Chronic Inflammation, published in Adv Sci (Weinh) (2025) — summary generated from the PubMed abstract.

Open my reading list
Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Adv Sci (Weinh) (2025)
Reported sample size
—
Source database
Europe PMC
PMID
40285666
PMCID
PMC12165033
DOI
10.1002/advs.202417489
Citations
2

Abstract (original English)

Atherosclerosis (AS) is a major pathological factor contributing to the mortality associated with ischemic heart disease and is driven primarily by macrophage-mediated lipid accumulation and inflammatory processes. Conventional cardiovascular pharmacotherapies address these pathological mechanisms but often show limited efficacy, highlighting the need for innovative agents capable of effectively reducing lipid accumulation and inflammation with minimal toxicity. In this study, decursin, a monomer derived from traditional Chinese medicine, is shown to inhibit both lipid accumulation and inflammatory responses in macrophages through direct interaction with protein kinase Cδ (PKCδ), resulting in low cytotoxicity in vitro and negligible toxicity in vivo. To address the short half-life of decursin, a targeted cascade drug delivery system (ALD@EM), which is specifically designed to target AS pathophysiology, is developed. This system employs ICAM-1 and VCAM-1 antibodies for plaque localization and incorporates low-density lipoproteins (LDLs) to facilitate chemotaxis to lesion sites, with an inner layer of apoptotic endothelial cell membranes to increase macrophage internalization and drug release. As a result, ALD@EM nanovesicles significantly increased the accumulation and therapeutic efficacy of decursin within plaques, substantially reducing lipid deposition and plaque inflammatio

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
MacrophagesAnimalsMice, Inbred C57BLHumansMiceButyratesBenzopyransDrug Delivery SystemsAtherosclerosisRAW 264.7 Cells

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.

Related research