Evidence map›Paper›PMID 26228924›Full record

ReviewThe Journal of physiology2016

Molecular mechanisms of hypoxia-inducible factor-induced pulmonary arterial smooth muscle cell alterations in pulmonary hypertension.

Christine Veith, Ralph T Schermuly, Ralf P Brandes, Norbert Weissmann

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  4. Roxadustat: Do we know all the answers?Biomolecules & biomedicine · 2023
    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

4 authors at 2 institutions in 1 country.

Christine VeithUniversities of Giessen and Marburg Lung Centre (UGMLC), member of the German Centre for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), 35392, Giessen, Germany.
Ralph T SchermulyUniversities of Giessen and Marburg Lung Centre (UGMLC), member of the German Centre for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), 35392, Giessen, Germany.
Ralf P BrandesInstitute for Cardiovascular Physiology, Goethe University Frankfurt, ECCPS, 60590, Frankfurt, Germany.
Norbert WeissmannUniversities of Giessen and Marburg Lung Centre (UGMLC), member of the German Centre for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), 35392, Giessen, Germany.
Universities of Giessen and Marburg Lung Center · DEGoethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxygen (O2) is essential for the viability and function of most metazoan organisms and thus is closely monitored at both the organismal and the cellular levels. However, alveoli often encounter decreased O2 levels (hypoxia), leading to activation of physiological or pathophysiological responses in the pulmonary arteries. Such changes are achieved by activation of transcription factors. The hypoxia-inducible factors (HIFs) are the most prominent hypoxia-regulated transcription factors in this regard. HIFs bind to hypoxia-response elements (HREs) in the promoter region of target genes, whose expression and translation allows the organism, amongst other factors, to cope with decreased environmental O2 partial pressure (pO2). However, prolonged HIF activation can contribute to major structural alterations, especially in the lung, resulting in the development of pulmonary hypertension (PH). PH is characterized by a rise in pulmonary arterial pressure associated with pulmonary arterial remodelling, concomitant with a reduced intravascular lumen area. Patients with PH develop right heart hypertrophy and eventually die from right heart failure. Thus, understanding the molecular mechanisms of HIF regulation in PH is critical for the identification of novel therapeutic strategies. This review addresses the relationship of hypoxia and the HIF system with pulmonary arterial dysfunction in PH. We particularly focus on the cellular and molecular mechanisms underlying the HIF-driven pathophysiological processes.

Indexed as

AnimalsHumansHypertension, PulmonaryHypoxia-Inducible Factor 1Myocytes, Smooth MuscleOxygenHypoxia-Inducible Factor 1Oxygen

Identifiers

PMID26228924
PMCPMC4771790
OpenAlexW2116775624

What OpenQuestion 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 OpenQuestion graph.