Evidence map›Paper›PMID 26424109›Full record

ReviewPflugers Archiv : European journal of physiology2016

NADPH oxidases-do they play a role in TRPC regulation under hypoxia?

Monika Malczyk, Christine Veith, Ralph T Schermuly, Thomas Gudermann, Alexander Dietrich, Natascha Sommer, Norbert Weissmann, Oleg Pak

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. The role of stretch-activated ion channels in acute respiratory distress syndrome: finally a new target?American journal of physiology. Lung cellular and molecular physiology · 2016
    Review
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

8 authors at 2 institutions in 1 country.

Monika MalczykUniversities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardiopulmonary System (ECCPS), Member of the German Center for Lung Research (DZL), Aulweg 130, 35392, Giessen, Germany.
Christine VeithUniversities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardiopulmonary System (ECCPS), Member of the German Center for Lung Research (DZL), Aulweg 130, 35392, Giessen, Germany.
Ralph T SchermulyUniversities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardiopulmonary System (ECCPS), Member of the German Center for Lung Research (DZL), Aulweg 130, 35392, Giessen, Germany.
Thomas GudermannWalther-Straub-Institute for Pharmacology and Toxicology, Ludwig-Maximilians University Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.
Alexander DietrichWalther-Straub-Institute for Pharmacology and Toxicology, Ludwig-Maximilians University Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.
Natascha SommerUniversities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardiopulmonary System (ECCPS), Member of the German Center for Lung Research (DZL), Aulweg 130, 35392, Giessen, Germany.
Norbert WeissmannUniversities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardiopulmonary System (ECCPS), Member of the German Center for Lung Research (DZL), Aulweg 130, 35392, Giessen, Germany. Norbert.Weissmann@innere.med.uni-giessen.de.
Oleg PakUniversities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardiopulmonary System (ECCPS), Member of the German Center for Lung Research (DZL), Aulweg 130, 35392, Giessen, Germany.
German Center for Lung Research · DEUniversities of Giessen and Marburg Lung Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the lung, acute alveolar hypoxia causes hypoxic pulmonary vasoconstriction (HPV) to maintain ventilation perfusion matching and thus optimal oxygenation of blood. In contrast, global chronic hypoxia triggers a pathological thickening of pulmonary arterial walls, called pulmonary vascular remodelling, leading to persistence of pulmonary hypertension (PH). Moreover, ischaemia or hypoxia can lead to a damage of pulmonary endothelial cells with subsequent oedema formation. Alterations in reactive oxygen species (ROS) have been suggested as a crucial mediator of such responses. Among the various sources of cellular ROS production, NADPH oxidases (NOXs) have been found to contribute to these physiological and pathophysiological signalling processes. NOXs are the only known examples that generate ROS as the primary function of the enzyme system. However, the downstream targets of NOX-derived ROS signalling in hypoxia are still not known. Canonical transient receptor potential (TRPC) channels recently have been recognised as directly or indirectly ROS-activated channels and have been shown to be essential for hypoxia-dependent vascular regulatory processes in the lung. Against this background, we here summarise the current knowledge on NOX-mediated TRPC channel signalling during hypoxia in the pulmonary circulation.

Indexed as

AnimalsHumansHypoxiaNADPH OxidasesReactive Oxygen SpeciesSignal TransductionTRPC Cation ChannelsNADPH OxidasesReactive Oxygen SpeciesTRPC Cation ChannelsHypoxic pulmonary vasoconstrictionNADPH oxidasesPulmonary hypertensionPulmonary vascular remodellingReactive oxygen speciesTransient receptor potential channels

Identifiers

PMID26424109
OpenAlexW2271695082

What Socratic holds

Textmetadata
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 Socratic graph.