Evidence map›Paper›PMID 32892378›Full record

ArticleAnnals of the New York Academy of Sciences2020

Transient receptor potential channels in pulmonary chemical injuries and as countermeasure targets.

Satyanarayana Achanta, Sven-Eric Jordt

Open access · greenAbstract read
In one paragraph

Article in Annals of the New York Academy of Sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. [Biomechanical properties of epithelial mesenchymal transition in idiopathic pulmonary fibrosis].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2023
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. TRPV4 Channel Modulators as Potential Drug Candidates for Cystic Fibrosis.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Countermeasures against Pulmonary Threat Agents.The Journal of pharmacology and experimental therapeutics · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. 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 at 1 institution in 1 country.

Satyanarayana AchantaDepartment of Anesthesiology, Duke University School of Medicine, Durham, North Carolina.ORCID 0000-0001-7121-5445
Sven-Eric JordtDepartment of Anesthesiology, Duke University School of Medicine, Durham, North Carolina.
Duke University · US

Funding

Advanced TRPA1 Inhibitor for the Treatment of Chlorine Inhalation InjuryU01ES030672 · NIEHS · DUKE UNIVERSITY · PI ACHANTA, SATYANARAYANA, JORDT, SVEN-ERIC · 2019 to 2021
$2.3M
Specialized pro-resolving mediators as potential medical countermeasures in a pig model of chlorine gas-induced acute lung injuryR21ES030331 · NIEHS · DUKE UNIVERSITY · PI ACHANTA, SATYANARAYANA, JORDT, SVEN-ERIC · 2020 to 2021
$443k
NIEHS, NIH Countermeasures Against Chemical Threat Agents (CounterACT) Program 1R21-ES030331-01A1NIEHS, NIH Countermeasures Against Chemical Threats (CounterACT) U01ES030672-01NIEHS NIH HHS R21 ES030331NIEHS NIH HHS U01 ES030672
6 · The paper itself

Abstract

The lung is highly sensitive to chemical injuries caused by exposure to threat agents in industrial or transportation accidents, occupational exposures, or deliberate use as weapons of mass destruction (WMD). There are no antidotes for the majority of the chemical threat agents and toxic inhalation hazards despite their use as WMDs for more than a century. Among several putative targets, evidence for transient receptor potential (TRP) ion channels as mediators of injury by various inhalational chemical threat agents is emerging. TRP channels are expressed in the respiratory system and are essential for homeostasis. Among TRP channels, the body of literature supporting essential roles for TRPA1, TRPV1, and TRPV4 in pulmonary chemical injuries is abundant. TRP channels mediate their function through sensory neuronal and nonneuronal pathways. TRP channels play a crucial role in complex pulmonary pathophysiologic events including, but not limited to, increased intracellular calcium levels, signal transduction, recruitment of proinflammatory cells, neurogenic inflammatory pathways, cough reflex, hampered mucus clearance, disruption of the integrity of the epithelia, pulmonary edema, and fibrosis. In this review, we summarize the role of TRP channels in chemical threat agents-induced pulmonary injuries and how these channels may serve as medical countermeasure targets for broader indications.

Indexed as

LungLung InjuryAnimalsCalciumCalcium SignalingChemical Warfare AgentsHumansTRPA1 Cation ChannelTRPV Cation ChannelsCalciumChemical Warfare AgentsTRPA1 Cation ChannelTRPA1 protein, humanTRPV1 protein, humanTRPV4 protein, humanTRPV Cation Channelsacute lung injurychlorine gasmedical countermeasurestear gas agentstoxic inhalation hazardsTRP ion channels

Identifiers

PMID32892378
PMCPMC7933981
OpenAlexW3083285711

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.