Evidence map›Paper›PMID 39656938›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Localized COUP-TFII pDNA Delivery Modulates Stem/Progenitor Cell Differentiation to Enhance Endothelialization and Inhibit Calcification of Decellularized Allografts.

Mengmeng Xing, Fei Wang, Ruowen Chu, He Wang, Yuyao Sun, Meng Qian, Huan Jiang, Adam C Midgley, Guohao Dai, Qiang Zhao

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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

10 authors.

Mengmeng XingState key Laboratory of Medicinal Chemical Biology, Frontiers Science Center for Cell Responses, Key Laboratory of Bioactive Materials (Ministry of Education), College of Life Sciences, Nankai University, Tianjin, 300071, China.
Fei WangState key Laboratory of Medicinal Chemical Biology, Frontiers Science Center for Cell Responses, Key Laboratory of Bioactive Materials (Ministry of Education), College of Life Sciences, Nankai University, Tianjin, 300071, China.
Ruowen ChuState key Laboratory of Medicinal Chemical Biology, Frontiers Science Center for Cell Responses, Key Laboratory of Bioactive Materials (Ministry of Education), College of Life Sciences, Nankai University, Tianjin, 300071, China.
He WangState key Laboratory of Medicinal Chemical Biology, Frontiers Science Center for Cell Responses, Key Laboratory of Bioactive Materials (Ministry of Education), College of Life Sciences, Nankai University, Tianjin, 300071, China.
Yuyao SunState key Laboratory of Medicinal Chemical Biology, Frontiers Science Center for Cell Responses, Key Laboratory of Bioactive Materials (Ministry of Education), College of Life Sciences, Nankai University, Tianjin, 300071, China.
Meng QianState key Laboratory of Medicinal Chemical Biology, Frontiers Science Center for Cell Responses, Key Laboratory of Bioactive Materials (Ministry of Education), College of Life Sciences, Nankai University, Tianjin, 300071, China.
Huan JiangState key Laboratory of Medicinal Chemical Biology, Frontiers Science Center for Cell Responses, Key Laboratory of Bioactive Materials (Ministry of Education), College of Life Sciences, Nankai University, Tianjin, 300071, China.
Adam C MidgleyState key Laboratory of Medicinal Chemical Biology, Frontiers Science Center for Cell Responses, Key Laboratory of Bioactive Materials (Ministry of Education), College of Life Sciences, Nankai University, Tianjin, 300071, China.
Guohao DaiDepartment of Bioengineering, Northeastern University, Boston, MA, 02115, USA.
Qiang ZhaoState key Laboratory of Medicinal Chemical Biology, Frontiers Science Center for Cell Responses, Key Laboratory of Bioactive Materials (Ministry of Education), College of Life Sciences, Nankai University, Tianjin, 300071, China.ORCID https://orcid.org/0000-0003-4656-6002

Funding

National Natural Science Foundation of China 81925021National Natural Science Foundation of China 82250610231National Natural Science Foundation of China 82330066
6 · The paper itself

Abstract

Decellularized allografts have emerged as promising candidates for vascular bypass grafting, owing to their inherent bioactivity and minimal immunogenicity. However, graft failure that results from suboptimal regeneration and pathological remodeling has hindered their clinical adoption. Recent advances in vascular biology highlight the pivotal role of COUP-TFII in orchestrating endothelial identity, angiogenesis, safeguarding against atherosclerosis, and mitigating vascular calcification. Here, plasmid DNA (pDNA) encoding COUP-TFII is incorporated into decellularized allografts to realize localized delivery. Comprehensive in vitro investigation complemented by a bone marrow transplantation model on genetic-lineage-tracing mouse revealed the underlying mechanisms of COUP-TFII in regulating vascular regeneration and remodeling. COUP-TFII augmented endothelialization and inhibited calcification in decellularized allografts by modulating the Ang1/Tie2/PI3K/AKT signaling pathway that dictates the fate of Sca-1

Indexed as

AllograftsCell DifferentiationStem CellsAnimalsDNAHumansMaleMiceMice, Inbred C57BLPlasmidsRatsDNAcalcificationCOUP‐TFIIdecellularized allograftsendothelial differentiationstem/progenitor cells (SPCs)

Identifiers

PMID39656938
PMCPMC11792037

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Registered trials

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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.