Evidence map›Paper›PMID 31379836›Full record

ReviewFrontiers in immunology2019

Purinergic Signaling in Pulmonary Inflammation.

Thanh-Thuy T Le, Nathaniel K Berg, Matthew T Harting, Xiangyun Li, Holger K Eltzschig, Xiaoyi Yuan

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
9.2field-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

74 citing papers in PubMed, 112 citations in OpenAlex.

  1. Endothelial c-IAP2 loss amplifies P2X7 receptor-driven inflammation and worsens schistosomiasis-associated pulmonary hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  18. Purinergic agonists increase [CaAmerican journal of physiology. Cell physiology · 2024
    Article
  19. Release of ATP in the lung evoked by inhalation of irritant gases in rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2024
    Article
  20. Review

14 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

Thanh-Thuy T LeDepartment of Anesthesiology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, United States.
Nathaniel K BergDepartment of Anesthesiology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, United States.
Matthew T HartingDepartment of Pediatric Surgery, McGovern Medical School, Children's Memorial Hermann Hospital, The University of Texas Health Science Center at Houston, Houston, TX, United States.
Xiangyun LiDepartment of Anesthesiology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, United States.
Holger K EltzschigDepartment of Anesthesiology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, United States.
Xiaoyi YuanDepartment of Anesthesiology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, United States.
The University of Texas Health Science Center at Houston · USMemorial Hermann · USTianjin Medical University · CN

Funding

Trangenic Mouse Breeding CoreP01HL114457 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ZHANG, YUJIN · 2013 to 2017
$10.0M
Novel Immunologic Effects of Semaphorin 7a in IPFR01HL109233 · NHLBI · YALE UNIVERSITY · PI HERZOG, ERICA L · 2011 to 2019
$3.7M
Hypoxia-Inducible Factors in Acetaminophen-Induced Liver Injury.R01DK109574 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ELTZSCHIG, HOLGER K., JU, CYNTHIA · 2016 to 2019
$1.8M
Proton Pump Inhibitors for Perioperative Acute Kidney InjuryR01DK097075 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ELTZSCHIG, HOLGER K. · 2013 to 2017
$1.7M
Amphiregulin Signaling in Perioperative Cardio-ProtectionR01HL119837 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ELTZSCHIG, HOLGER K. · 2014 to 2017
$1.5M
MicroRNA Shuttling during Acute Respiratory Distress SyndromeR01HL133900 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ELTZSCHIG, HOLGER K. · 2017 to 2020
$1.5M
Training Interdisciplinary Pharmacology ScientistsT32GM120011 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DESSAUER, CARMEN W. · 2016 to 2020
$1.0M
NHLBI NIH HHS P01 HL114457NHLBI NIH HHS R01 HL109233NHLBI NIH HHS R01 HL119837NHLBI NIH HHS R01 HL133900NIDDK NIH HHS R01 DK097075NIDDK NIH HHS R01 DK109574NIGMS NIH HHS T32 GM120011
6 · The paper itself

Abstract

Purine nucleotides and nucleosides are at the center of biologic reactions. In particular, adenosine triphosphate (ATP) is the fundamental energy currency of cellular activity and adenosine has been demonstrated to play essential roles in human physiology and pathophysiology. In this review, we examine the role of purinergic signaling in acute and chronic pulmonary inflammation, with emphasis on ATP and adenosine. ATP is released into extracellular space in response to cellular injury and necrosis. It is then metabolized to adenosine monophosphate (AMP) via ectonucleoside triphosphate diphosphohydrolase-1 (CD39) and further hydrolyzed to adenosine via ecto-5'-nucleotidase (CD73). Adenosine signals via one of four adenosine receptors to exert pro- or anti-inflammatory effects. Adenosine signaling is terminated by intracellular transport by concentrative or equilibrative nucleoside transporters (CNTs and ENTs), deamination to inosine by adenosine deaminase (ADA), or phosphorylation back into AMP via adenosine kinase (AK). Pulmonary inflammatory and hypoxic conditions lead to increased extracellular ATP, adenosine diphosphate (ADP) and adenosine levels, which translates to increased adenosine signaling. Adenosine signaling is central to the pulmonary injury response, leading to various effects on inflammation, repair and remodeling processes that are either tissue-protective or tissue destructive. In the acute setting, particularly through activation of adenosine 2A and 2B receptors, adenosine signaling serves an anti-inflammatory, tissue-protective role. However, excessive adenosine signaling in the chronic setting promotes pro-inflammatory, tissue destructive effects in chronic pulmonary inflammation.

Indexed as

Adenosine DeaminaseAdenosine MonophosphateAdenosine TriphosphateAnimalsHumansPneumoniaPurinergic AgentsSignal TransductionAdenosine DeaminaseAdenosine MonophosphateAdenosine TriphosphatePurinergic Agentsacute pulmonary inflammationadenosinechronic pulmonary inflammationectonucleotidasenucleotidespurinergic signaling

Identifiers

PMID31379836
PMCPMC6646739
OpenAlexW2957308520

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.