ReviewFrontiers in pediatrics2024
Post-translational modifications and bronchopulmonary dysplasia.
Review in Frontiers in pediatrics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled 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.
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
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Elevated HMGB1 Levels in Neonates With Bronchopulmonary Dysplasia: A Systematic Review and Meta-Analysis.Canadian respiratory journal · 2026Pooled it
- Targeting the SIRT1-TLR4 axis attenuates oxidative inflammation in a cellular model of bronchopulmonary dysplasia.Pediatric research · 2026Article
- Mapping the evolving landscape: a bibliometric analysis of macrophages research in bronchopulmonary dysplasia (1990-2025)-a Web of Science Core Collection-based study.Translational pediatrics · 2026Article
- MOTS-c: How a secreted mitochondrial microprotein may become a potential treatment for inflammatory lung diseases.Journal of translational medicine · 2026Review
- Endothelial SP1 lactylation promotes bronchopulmonary dysplasia via regulation of Cdkn1a expression.Scientific reports · 2026Article
- GINS4 Promotes Neonatal Bronchopulmonary Dysplasia via Driving Phosphorylation and Acetylation of p65 NF-κB.Molecular biotechnology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bronchopulmonary dysplasia is a prevalent respiratory disorder posing a significant threat to the quality of life in premature infants. Its pathogenesis is intricate, and therapeutic options are limited. Besides genetic coding, protein post-translational modification plays a pivotal role in regulating cellular function, contributing complexity and diversity to substrate proteins and influencing various cellular processes. Substantial evidence indicates that post-translational modifications of several substrate proteins are intricately related to the molecular mechanisms underlying bronchopulmonary dysplasia. These modifications facilitate the progression of bronchopulmonary dysplasia through a cascade of signal transduction events. This review outlines the relationships between substrate protein phosphorylation, acetylation, ubiquitination, SUMOylation, methylation, glycosylation, glycation, S-glutathionylation, S-nitrosylation and bronchopulmonary dysplasia. The aim is to provide novel insights into bronchopulmonary dysplasia's pathogenesis and potential therapeutic targets for clinical management.
Indexed as
Identifiers
What 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.