Evidence map›Paper›PMID 41577699›Full record

ArticleScientific reports2026

A high-performance hydrogel platform enabling dual anti-miR-21 and TGF-β1 delivery to improve arterial plaque stability and enhance therapeutic angiogenesis outcomes.

Paromita Islam, Ahmed Abosalha, Sabrina Schaly, Jacqueline L Boyajian, Amal Kassab, Stephanie Makhlouf, Madison Santos, Editha Renesteen, Cedrique Shum-Tim, Arghya Pal and 2 more

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Paromita IslamBiomedical Technology and Cell Therapy Research Laboratory, Department of Biomedical Engineering, Faculty of Medicine and Health Sciences, McGill University, Montreal, QC, H3A 2B4, Canada.
Ahmed AbosalhaBiomedical Technology and Cell Therapy Research Laboratory, Department of Biomedical Engineering, Faculty of Medicine and Health Sciences, McGill University, Montreal, QC, H3A 2B4, Canada.
Sabrina SchalyBiomedical Technology and Cell Therapy Research Laboratory, Department of Biomedical Engineering, Faculty of Medicine and Health Sciences, McGill University, Montreal, QC, H3A 2B4, Canada.
Jacqueline L BoyajianBiomedical Technology and Cell Therapy Research Laboratory, Department of Biomedical Engineering, Faculty of Medicine and Health Sciences, McGill University, Montreal, QC, H3A 2B4, Canada.
Amal KassabBiomedical Technology and Cell Therapy Research Laboratory, Department of Biomedical Engineering, Faculty of Medicine and Health Sciences, McGill University, Montreal, QC, H3A 2B4, Canada.
Stephanie MakhloufBiomedical Technology and Cell Therapy Research Laboratory, Department of Biomedical Engineering, Faculty of Medicine and Health Sciences, McGill University, Montreal, QC, H3A 2B4, Canada.
Madison SantosBiomedical Technology and Cell Therapy Research Laboratory, Department of Biomedical Engineering, Faculty of Medicine and Health Sciences, McGill University, Montreal, QC, H3A 2B4, Canada.
Editha RenesteenBiomedical Technology and Cell Therapy Research Laboratory, Department of Biomedical Engineering, Faculty of Medicine and Health Sciences, McGill University, Montreal, QC, H3A 2B4, Canada.
Cedrique Shum-TimBiomedical Technology and Cell Therapy Research Laboratory, Department of Biomedical Engineering, Faculty of Medicine and Health Sciences, McGill University, Montreal, QC, H3A 2B4, Canada.
Arghya PalDepartment of Chemical and Biochemical Engineering, Western University, London, ON, N6A 5B9, Canada.
Dominique Shum-TimDivision of Cardiac Surgery, Faculty of Medicine and Health Sciences, McGill University Health Centre, Royal Victoria Hospital, McGill University, Montreal, QC, H3G 2M1, Canada.
Satya PrakashBiomedical Technology and Cell Therapy Research Laboratory, Department of Biomedical Engineering, Faculty of Medicine and Health Sciences, McGill University, Montreal, QC, H3A 2B4, Canada. satya.prakash@mcgill.ca.

Funding

CIHR 252743Islamic Development Bank Scholarship 2020-245622Natural Sciences and Engineering Research Council 569661-2022
6 · The paper itself

Abstract

Atherosclerosis is the primary cause of most cases of coronary artery disease, peripheral arterial disease, and many strokes. It is characterized by pathological vascular smooth muscle cell hyperplasia. Current treatment regimens are associated with several adverse effects including hepatotoxicity, hemorrhagic complications, and non-selective cellular inhibition. Plaque stabilization and angiogenesis are critical for mitigating adverse cardiovascular outcomes. Stabilized plaques exhibit reduced vulnerability to rupture, thereby lowering the risk of thrombus formation, myocardial infarction, and ischemic stroke. Transforming Growth Factor Beta 1 (TGF-β1cells) is instrumental in promoting angiogenesis, facilitating the regrowth of endothelial cells, and contributing to the stabilization of atherosclerotic plaques. Anti-miRNA 21 can lead to plaque stabilization by decreasing inflammation and limiting the growth of smooth muscle cells while encouraging cell death, which helps prevent plaque rupture. This research investigates a novel combination therapy utilizing anti-miR-21 and baculovirus expressing TGF-β1 gene for vascular tissue regeneration. A hemocompatible nanocomposite hydrogel with remarkable cellular adhesion profile was prepared by encapsulating anti-miR-21 and baculovirus expressing TGF-β1 gene in PLGA nanoparticles, followed by embedding them in a gelatin-genipin crosslinked nanocomposite hydrogel. Chorioallantoic membrane assay in chicken embryo and PTEN quantification study was used for angiogenesis. MTT assay followed by Annexin V-FITC/PI stained flowcytometry was used for HASMCs apoptosis study. The combination therapy demonstrates synergistic effects through dual mechanisms: promoting neo-vascularization via selective endothelial cell proliferation while inducing arterial smooth muscle cell apoptosis (22.27 ± 1.2%) to control extracellular matrix secretion and stabilize plaque. The therapeutic efficacy is evidenced by significant reduction in PTEN expression (251.1 ±16 pg/ml compared to 375.2 ± 5.29 pg/ml in control) and enhanced angiogenic responses in the CAM assay, showing a 126.46 ± 16.62% increase in vessel length.

Indexed as

AngiogenesisHydrogelsMicroRNAsNeovascularization, PathologicNeovascularization, PhysiologicPlaque, AtheroscleroticTransforming Growth Factor beta1AnimalsHumansMyocytes, Smooth MusclePTEN PhosphohydrolaseHydrogelsMicroRNAsPTEN PhosphohydrolaseTransforming Growth Factor beta1AngiogenesisApoptosis.AtherosclerosisBaculovirusGene therapyHydrogelNanoparticleTissue regenerationViral vector

Identifiers

PMID41577699
PMCPMC12835175

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.