ArticleVessel plus2018
Histone deacetylases in vascular permeability and remodeling associated with acute lung injury.
Article in Vessel plus, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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
10 citing papers in PubMed, 11 citations in OpenAlex.
- Mechanisms of pulmonary endothelial barrier dysfunction in acute lung injury and acute respiratory distress syndrome.Chinese medical journal pulmonary and critical care medicine · 2024Article
- Zinc-Dependent Histone Deacetylases in Lung Endothelial Pathobiology.Biomolecules · 2024Review
- The Role of Histone Deacetylases in Acute Lung Injury-Friend or Foe.International journal of molecular sciences · 2023Review
- HDAC6 Activates ERK in Airway and Pulmonary Vascular Remodeling of Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2021Article
- Identification of early and intermediate biomarkers for ARDS mortality by multi-omic approaches.Scientific reports · 2021Observational
- HDAC inhibitor, MS-275, increases vascular permeability by suppressing Robo4 expression in endothelial cells.Tissue barriers · 2021Article
- Inhibition of Class IIa HDACs improves endothelial barrier function in endotoxin-induced acute lung injury.Journal of cellular physiology · 2021Article
- Molecular Mechanisms of Vascular Damage During Lung Injury.Advances in experimental medicine and biology · 2021Review
- Microtubules as Major Regulators of Endothelial Function: Implication for Lung Injury.Frontiers in physiology · 2021Review
- Vascular remodeling 2018: the updates.Vessel plus · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Acute lung injury (ALI) is a severe progressive disorder that arises from a wide range of causes such as toxins or inflammation, resulting in significant morbidity and mortality. There are no effective therapeutic options apart from mechanical ventilation strategies. While the mechanisms that govern the clinically relevant process of increased EC permeability and remodeling associated with ALI are under intense investigation, our knowledge of the processes that determine barrier enhancement or preservation are far from completion. Recently, epigenetic mechanisms have emerged as a major regulator of enduring changes in cell behavior and the therapeutic potential of inhibiting histone deacetylases (HDACs) for the treatment of cardiovascular and inflammatory diseases has gained remarkable attention. Although HDACs have been shown to play an important role in regulating EC barrier function, the involved HDAC subtypes and mechanisms remain undefined. Further investigation of the HDAC signaling may provide therapeutic approaches for the prevention and treatment of ALI.
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.