Evidence map›Paper›PMID 38345908›Full record

ReviewAnnual review of physiology2024

A Razor's Edge: Vascular Responses to Acute Inflammatory Lung Injury/Acute Respiratory Distress Syndrome.

David R Price, Joe G N Garcia

Abstract readReview
In one paragraph

Review in Annual review of physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
–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

18 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  8. Lung Lymphatics in Edema, Inflammation, and Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
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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

2 authors.

David R PriceDepartment of Medicine, Division of Pulmonary and Critical Care Medicine, New York-Presbyterian Hospital/Weill Cornell Medical Center, New York, NY, USA.
Joe G N GarciaCenter for Inflammation Sciences and Systems Medicine, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Jupiter, Florida, USA; email: jgn.garcia@ufl.edu.

Funding

Structure-Function Analysis of nmMLCK in EC Barrier ResponsesP01HL126609 · NHLBI · UNIVERSITY OF FLORIDA · PI Nathan A. Ellis · 2016 to 2026
$24.4M
Novel Involvement of NAMPT and TLR4 in PAH Vascular RemodelingR01HL141387 · NHLBI · UNIVERSITY OF FLORIDA · PI Joe G. N. Garcia, Ayako Makino · 2019 to 2026
$3.8M
A Randomized Phase 2A Clinical Trial Pioneering the Utility of an eNAMPT-Reducing Therapy in ARDS/VILI: the PUERTA TrialR44HL145930 · NHLBI · AQUALUNG THERAPEUTICS CORP. · PI GARCIA, JOE G. N. · 2023 to 2024
$2.5M
Preclinical Development of a Novel eNAMPT-Neutralizing mAb for Pulmonary HypertensionR42HL164300 · NHLBI · AQUALUNG THERAPEUTICS CORP. · PI GARCIA, JOE G. N. · 2022 to 2024
$1.9M
Protective role of Endothelial Receptor Interacting Protein Kinase 3 (RIPK3) in acute lung injuryK08HL166958 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI DAVID REGAN PRICE · 2024 to 2026
$507k
Validation of a Genetic-based Biomarker Panel for Stratification of Mortality Risk in ARDS PatientsR21HL168142 · NHLBI · UNIVERSITY OF ARIZONA · PI BIME, CHRISTIAN, GARCIA, JOE G. N. · 2023 to 2023
$115k
NHLBI NIH HHS K08 HL166958NHLBI NIH HHS P01 HL126609NHLBI NIH HHS R01 HL141387NHLBI NIH HHS R21 HL168142NHLBI NIH HHS R42 HL164300NHLBI NIH HHS R44 HL145930
6 · The paper itself

Abstract

Historically considered a metabolically inert cellular layer separating the blood from the underlying tissue, the endothelium is now recognized as a highly dynamic, metabolically active tissue that is critical to organ homeostasis. Under homeostatic conditions, lung endothelial cells (ECs) in healthy subjects are quiescent, promoting vasodilation, platelet disaggregation, and anti-inflammatory mechanisms. In contrast, lung ECs are essential contributors to the pathobiology of acute respiratory distress syndrome (ARDS), as the quiescent endothelium is rapidly and radically altered upon exposure to environmental stressors, infectious pathogens, or endogenous danger signals into an effective and formidable regulator of innate and adaptive immunity. These dramatic perturbations, produced in a tsunami of inflammatory cascade activation, result in paracellular gap formation between lung ECs, sustained lung edema, and multi-organ dysfunction that drives ARDS mortality. The astonishing plasticity of the lung endothelium in negotiating this inflammatory environment and efforts to therapeutically target the aberrant ARDS endothelium are examined in further detail in this review.

Indexed as

Lung InjuryRespiratory Distress SyndromeEndothelial CellsEndothelium, VascularHomeostasisHumansLungacute respiratory distress syndromeARDScell deathendotheliuminflammationinnate immunityvascular responses

Identifiers

PMID38345908
PMCPMC11259086

What OpenQuestion holds

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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.