Evidence map›Paper›PMID 34019265›Full record

ReviewAdvances in experimental medicine and biology2021

Molecular Mechanisms of Vascular Damage During Lung Injury.

Ramon Bossardi Ramos, Alejandro Pablo Adam

Open access · greenAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
25.1field-weighted citation impact, top 1% of its field
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

24 citing papers in PubMed, 32 citations in OpenAlex.

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  12. Alveolar macrophages polarization switch via αInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  20. Ceapin-A7 potentiates lipopolysaccharide-induced endothelial injury.Journal of biochemical and molecular toxicology · 2023
    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

2 authors at 1 institution in 1 country.

Ramon Bossardi RamosDepartment of Molecular and Cellular Physiology, Albany Medical College, Albany, NY, USA. bossarr@amc.edu.
Alejandro Pablo AdamDepartment of Molecular and Cellular Physiology, Albany Medical College, Albany, NY, USA. adama1@amc.edu.
Albany Medical Center Hospital · US

Funding

Role of endothelial JAK/STAT signaling in the regulation of vascular leakageR01GM124133 · NIGMS · ALBANY MEDICAL COLLEGE · PI ADAM, ALEJANDRO PABLO · 2018 to 2022
$2.2M
NIGMS NIH HHS R01 GM124133
6 · The paper itself

Abstract

A variety of pulmonary and systemic insults promote an inflammatory response causing increased vascular permeability, leading to the development of acute lung injury (ALI), a condition necessitating hospitalization and intensive care, or the more severe acute respiratory distress syndrome (ARDS), a disease with a high mortality rate. Further, COVID-19 pandemic-associated ARDS is now a major cause of mortality worldwide. The pathogenesis of ALI is explained by injury to both the vascular endothelium and the alveolar epithelium. The disruption of the lung endothelial and epithelial barriers occurs in response to both systemic and local production of pro-inflammatory cytokines. Studies that evaluate the association of genetic polymorphisms with disease risk did not yield many potential therapeutic targets to treat and revert lung injury. This failure is probably due in part to the phenotypic complexity of ALI/ARDS, and genetic predisposition may be obscured by the multiple environmental and behavioral risk factors. In the last decade, new research has uncovered novel epigenetic mechanisms that control ALI/ARDS pathogenesis, including histone modifications and DNA methylation. Enzyme inhibitors such as DNMTi and HDACi may offer new alternative strategies to prevent or reverse the vascular damage that occurs during lung injury. This review will focus on the latest findings on the molecular mechanisms of vascular damage in ALI/ARDS, the genetic factors that might contribute to the susceptibility for developing this disease, and the epigenetic changes observed in humans, as well as in experimental models of ALI/ADRS.

Indexed as

Acute Lung InjuryCOVID-19Respiratory Distress SyndromeHumansLungPandemicsSARS-CoV-2Lung injury; Vascular damage; Epithelial barrier; Endothelial activation; Epigenetics; Histone acetylation, DNA methylation; Inflammation

Identifiers

PMID34019265
PMCPMC8223730
OpenAlexW3163823657

What OpenQuestion holds

Textmetadata
LicenceTDM
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.