Evidence map›Paper›PMID 21691314›Full record

ReviewNature reviews. Cardiology2011

Mechanisms of disease: pulmonary arterial hypertension.

Ralph T Schermuly, Hossein A Ghofrani, Martin R Wilkins, Friedrich Grimminger

Abstract readReview
In one paragraph

Review in Nature reviews. Cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 406 papers.

0numbers the graph read from it
0cells of the map it votes in
406citing papers in PubMed
–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

406 citing papers in PubMed.

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346 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

4 authors.

Ralph T SchermulyMax-Planck-Institute for Heart and Lung Research, Parkstrasse 1, 61231 Bad Nauheim, Germany. ralph.schermuly@ innere.med. uni-giessen.de
Hossein A Ghofrani
Martin R Wilkins
Friedrich Grimminger

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our understanding of, and approach to, pulmonary arterial hypertension has undergone a paradigm shift in the past decade. Once a condition thought to be dominated by increased vasoconstrictor tone and thrombosis, pulmonary arterial hypertension is now seen as a vasculopathy in which structural changes driven by excessive vascular cell growth and inflammation, with recruitment and infiltration of circulating cells, play a major role. Perturbations of a number of molecular mechanisms have been described, including pathways involving growth factors, cytokines, metabolic signaling, elastases, and proteases, that may underlie the pathogenesis of the disease. Elucidating their contribution to the pathophysiology of pulmonary arterial hypertension could offer new drug targets. The role of progenitor cells in vascular repair is also under active investigation. The right ventricular response to increased pressure load is recognized as critical to survival and the molecular mechanisms involved are attracting increasing interest. The challenge now is to integrate this new knowledge and explore how it can be used to categorize patients by molecular phenotype and tailor treatment more effectively.

Indexed as

AnimalsBlood CoagulationCell ProliferationEndothelial CellsFamilial Primary Pulmonary HypertensionHemodynamicsHumansHypertension, PulmonaryInflammation MediatorsNeovascularization, PhysiologicSignal TransductionInflammation Mediators

Identifiers

PMID21691314
PMCPMC7097518

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.