ArticleDrug delivery and translational research2026
Platelet membrane-fusing MSC-derived apoptotic extracellular vesicles enhanced cardiac repair after ischemia/reperfusion injury.
Article in Drug delivery and translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Myocardial ischemia/reperfusion injury (I/RI) is a common complication following percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI). Mesenchymal stem cell-derived apoptotic vesicles (MSC-apoVs) seem to be a promising cell-free therapy for alleviating cardiac I/RI, but their therapeutic efficiency is hindered by insufficient targeting capability in vivo. The present study aims to explore the platelet membrane-modified apoVs (P-apoVs), utilizing the nature affinity of platelets for apoV delivery to the injured vascular and myocardial sites. P-apoVs exhibited excellent physicochemical properties, and microRNA (miRNA)-sequencing showed that the extrusion process had no detrimental effects on the content and distribution of miRNAs. Compared to non-modified apoVs, the cellular uptake of P-apoVs was greatly enhanced in bone marrow-derived macrophages (BMDMs), human umbilical vein endothelial cells (HUVECs) stressed by oxygen glucose deprivation/reperfusion (OGD/R) and neonatal rat cardiomyocytes (NRCMs) stressed by OGD/R. Functionally, P-apoVs inhibited the apoptosis of OGD/R NRCMs, promoted BMDM polarization toward M2 phenotype, as well as enhanced HUVEC migration and tube formation in vitro. In the myocardial I/RI model, P-apoVs preferentially accumulated in the injured myocardial sites and attenuate cardiac modeling after I/RI without systemic toxicity. In conclusion, this engineering platelet-modified apoVs shows potential as a therapeutic strategy for myocardial I/RI.
Indexed as
Identifiers
42479341What OpenQuestion 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 OpenQuestion graph.