Evidence map›Paper›PMID 42752987›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Developing Highly Effective Nanoparticle mRNA Therapeutic for Pediatric Acute Respiratory Distress Syndrome.

Zicheng Deng, Wen Gao, Jonathan Do, Danli Lu, Ying-Wei Lan, Andreas Damianos, Gautam Verma, Ali Al Siraj, Isabella Lowry, Lance Peter and 5 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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

15 authors.

Zicheng DengPhoenix Children's Research Institute, Department of Child Health, University of Arizona College of Medicine, Phoenix, United State.ORCID https://orcid.org/0000-0001-6868-7927
Wen GaoPhoenix Children's Research Institute, Department of Child Health, University of Arizona College of Medicine, Phoenix, United State.ORCID https://orcid.org/0000-0002-7241-7900
Jonathan DoPhoenix Children's Research Institute, Department of Child Health, University of Arizona College of Medicine, Phoenix, United State.ORCID https://orcid.org/0009-0003-5043-2936
Danli LuPhoenix Children's Research Institute, Department of Child Health, University of Arizona College of Medicine, Phoenix, United State.
Ying-Wei LanPhoenix Children's Research Institute, Department of Child Health, University of Arizona College of Medicine, Phoenix, United State.
Andreas DamianosPhoenix Children's Research Institute, Department of Child Health, University of Arizona College of Medicine, Phoenix, United State.ORCID https://orcid.org/0009-0005-4326-8749
Gautam VermaPhoenix Children's Research Institute, Department of Child Health, University of Arizona College of Medicine, Phoenix, United State.
Ali Al SirajPhoenix Children's Research Institute, Department of Child Health, University of Arizona College of Medicine, Phoenix, United State.
Isabella LowryPhoenix Children's Research Institute, Department of Child Health, University of Arizona College of Medicine, Phoenix, United State.
Lance PeterDivision of Bioinnovation and Genome Sciences, Translational Genomics Research Institute, United State.
Nicholas E BanovichDivision of Bioinnovation and Genome Sciences, Translational Genomics Research Institute, United State.
Fei SunKey Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, China.
Hua HeKey Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, China.
Tanya V KalinPhoenix Children's Research Institute, Department of Child Health, University of Arizona College of Medicine, Phoenix, United State.ORCID https://orcid.org/0000-0002-8545-8277
Vladimir V KalinichenkoPhoenix Children's Research Institute, Department of Child Health, University of Arizona College of Medicine, Phoenix, United State.ORCID https://orcid.org/0000-0003-3438-2660

Funding

Transcriptional Regulation of Endothelial Cells after Neonatal Lung InjuryR01HL141174 · NHLBI · UNIVERSITY OF ARIZONA · PI Vladimir Kalinichenko · 2018 to 2026
$4.7M
Development of novel therapeutic approaches for treatment of Alveolar Capillary DysplasiaR01HL152973 · NHLBI · UNIVERSITY OF ARIZONA · PI Vladimir Kalinichenko · 2021 to 2026
$3.6M
Molecular Mechanisms Regulated by FOXM1 in Chronic Lung RemodelingR01HL149631 · NHLBI · UNIVERSITY OF ARIZONA · PI KALINICHENKO, VLADIMIR · 2020 to 2022
$2.2M
Developing Nanoplatforms for Co-Delivery of Drugs and Genes to Protect Lung Endothelium from InjuryK99HL188210 · NHLBI · UNIVERSITY OF ARIZONA · PI Zicheng Deng · 2026 to 2026
$109k
National Institutes of Health (NIH) HL141174National Institutes of Health (NIH) HL149631National Institutes of Health (NIH) HL152973National Institutes of Health (NIH) HL188210NHLBI NIH HHS K99 HL188210NHLBI NIH HHS R01 HL141174NHLBI NIH HHS R01 HL149631NHLBI NIH HHS R01 HL152973
6 · The paper itself

Abstract

Sepsis-induced pediatric acute lung injury (ALI) and pediatric acute respiratory distress syndrome (PARDS) are life-threatening conditions with high mortality rates and no current cure. Most ALI/ARDS studies focus on adults, albeit the pediatric population has unique challenges often underrepresented. ALI/PARDS severely impacts pulmonary endothelial cells (ECs), causing endothelial dysfunction and vascular leakage. FOXF1 is a transcription factor critical for lung repair after injury, representing a viable target for ALI/PARDS. This study developed and tested a novel nanoparticle system for precise delivery of FOXF1 mRNA into lung ECs to reduce endothelial damage and improve lung function in mouse model of PARDS. Systemic inflammatory response was induced in neonatal mice after intraperitoneal administration of lipopolysaccharide (LPS). Specifically designed nanoparticles (NP) were used to intravenously deliver stabilized FOXF1 mRNA (FOXF1 NP) after LPS injury to restore FOXF1 expression in injured lung endothelial cells. FOXF1 NP selectively targeted pulmonary ECs without affecting other cell types or organs. FOXF1 NP treatment reduced vascular leakage, enhanced endothelial barrier function, and improved survival of neonatal mice after injury. FOXF1 NP decreased EC apoptosis by restoring the expression of BCL2, an anti-apoptotic FOXF1 target gene. Nanoparticle-based rescue of lung ECs has promise for future treatments of human ALI/PARDS.

Indexed as

endothelial cellsgene therapynanoparticle delivery systempediatric acute respiratory distress syndromesepsis

Identifiers

PMID42752987
PMCPMC13584808

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.