Evidence map›Paper›PMID 38709389›Full record

ArticleAngiogenesis2024

IC100, a humanized therapeutic monoclonal anti-ASC antibody alleviates oxygen-induced retinopathy in mice.

Huijun Yuan, Shaoyi Chen, Matthew R Duncan, Juan Pablo de Rivero Vaccari, Robert W Keane, W Dalton Dietrich, Tsung-Han Chou, Merline Benny, Augusto F Schmidt, Karen Young and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Angiogenesis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Inflammasomes in glioblastoma.Journal of neuroinflammation · 2026
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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

14 authors.

Huijun YuanDepartment of Pediatrics/Division of Neonatology, Batchelor Children's Research Institute and Holtz Children's Hospital, University of Miami Miller School of Medicine, P. O. Box 016960, Miami, FL, 33101, USA.
Shaoyi ChenDepartment of Pediatrics/Division of Neonatology, Batchelor Children's Research Institute and Holtz Children's Hospital, University of Miami Miller School of Medicine, P. O. Box 016960, Miami, FL, 33101, USA.
Matthew R DuncanDepartment of Pediatrics/Division of Neonatology, Batchelor Children's Research Institute and Holtz Children's Hospital, University of Miami Miller School of Medicine, P. O. Box 016960, Miami, FL, 33101, USA.
Juan Pablo de Rivero VaccariThe Miami Project to Cure Paralysis and Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL, USA.
Robert W KeaneThe Miami Project to Cure Paralysis and Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL, USA.
W Dalton DietrichThe Miami Project to Cure Paralysis and Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL, USA.
Tsung-Han ChouBascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL, USA.
Merline BennyDepartment of Pediatrics/Division of Neonatology, Batchelor Children's Research Institute and Holtz Children's Hospital, University of Miami Miller School of Medicine, P. O. Box 016960, Miami, FL, 33101, USA.
Augusto F SchmidtDepartment of Pediatrics/Division of Neonatology, Batchelor Children's Research Institute and Holtz Children's Hospital, University of Miami Miller School of Medicine, P. O. Box 016960, Miami, FL, 33101, USA.
Karen YoungDepartment of Pediatrics/Division of Neonatology, Batchelor Children's Research Institute and Holtz Children's Hospital, University of Miami Miller School of Medicine, P. O. Box 016960, Miami, FL, 33101, USA.
Kevin K ParkDepartment of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Vittorio PorciattiBascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL, USA.
M Elizabeth HartnettByers Eye Institute at Stanford University, Palo Alto, CA, USA.
Shu WuDepartment of Pediatrics/Division of Neonatology, Batchelor Children's Research Institute and Holtz Children's Hospital, University of Miami Miller School of Medicine, P. O. Box 016960, Miami, FL, 33101, USA. swu2@med.miami.edu.

Funding

Exosomal Gasdermin D Mediated Lung to Brain Crosswalk in Preterm Brain InjuryR01HL156803 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI WU, SHU · 2020 to 2023
$2.4M
NHLBI NIH HHS 1R01HL156803NHLBI NIH HHS R01 HL156803
6 · The paper itself

Abstract

backgroundRetinopathy of prematurity (ROP), which often presents with bronchopulmonary dysplasia (BPD), is among the most common morbidities affecting extremely premature infants and is a leading cause of severe vision impairment in children worldwide. Activations of the inflammasome cascade and microglia have been implicated in playing a role in the development of both ROP and BPD. Apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) is pivotal in inflammasome assembly. Utilizing mouse models of both oxygen-induced retinopathy (OIR) and BPD, this study was designed to test the hypothesis that hyperoxia induces ASC speck formation, which leads to microglial activation and retinopathy, and that inhibition of ASC speck formation by a humanized monoclonal antibody, IC100, directed against ASC, will ameliorate microglial activation and abnormal retinal vascular formation.

methodsWe first tested ASC speck formation in the retina of ASC-citrine reporter mice expressing ASC fusion protein with a C-terminal citrine (fluorescent GFP isoform) using a BPD model that causes both lung and eye injury by exposing newborn mice to room air (RA) or 85% O

resultsASC specks were significantly increased in the retinas by hyperoxia exposure and colocalized with the abnormal vasculature in both BPD and OIR models, and this was associated with increased microglial activation. Treatment with IC100-IVT or IC100-IP significantly reduced vaso-obliteration and intravitreal neovascularization. IC100-IVT treatment also reduced retinal microglial activation, restored retinal structure, and improved retinal function. RNA-seq showed that IC100 treatment corrected the induction of genes associated with angiogenesis, leukocyte migration, and VEGF signaling caused by O

conclusionThese data demonstrate the crucial role of ASC in the pathogenesis of OIR and the efficacy of a humanized therapeutic anti-ASC antibody in treating OIR mice. Thus, this anti-ASC antibody may potentially be considered in diseases associated with oxygen stresses and retinopathy, such as ROP.

Indexed as

OxygenRetinopathy of PrematurityAnimalsAnimals, NewbornAntibodies, Monoclonal, HumanizedCARD Signaling Adaptor ProteinsDisease Models, AnimalHumansHyperoxiaMiceMice, Inbred C57BLMice, TransgenicMicrogliaRetinaRetinal NeovascularizationAntibodies, Monoclonal, HumanizedCARD Signaling Adaptor ProteinsOxygenASCIC100MicrogliaOxygen-induced retinopathyTranscriptome

Identifiers

PMID38709389
PMCPMC11303442

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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.