Evidence map›Paper›PMID 23202738›Full record

ReviewThe Journal of clinical investigation2012

Molecular pathogenesis of pulmonary arterial hypertension.

Marlene Rabinovitch

Abstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 373 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
373citing papers in PubMed, 2 pooled it
–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

373 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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313 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

1 author.

Marlene RabinovitchStanford University School of Medicine, Stanford, California 94305-5162, USA. marlener@stanford.edu

Funding

The Cellular Response to Elafin in PAHP01HL108797 · NHLBI · STANFORD UNIVERSITY · PI NOLAN, GARRY P · 2011 to 2021
$19.7M
Pulmonary Hypertension in Genetically Modified MiceR01HL074186 · NHLBI · STANFORD UNIVERSITY · PI RABINOVITCH, MARLENE · 2004 to 2022
$10.4M
NHLBI NIH HHS P01 HL108797NHLBI NIH HHS R01 HL074186
6 · The paper itself

Abstract

Recent clinical and experimental studies are redefining the cellular and molecular bases of pulmonary arterial hypertension (PAH). The genetic abnormalities first identified in association with the idiopathic form of PAH--together with a vast increase in our understanding of cell signaling, cell transformation, and cell-cell interactions; gene expression; microRNA processing; and mitochondrial and ion channel function--have helped explain the abnormal response of vascular cells to injury. Experimental and clinical studies now converge on the intersection and interactions between a genetic predisposition involving the BMPR2 signaling pathway and an impaired metabolic and chronic inflammatory state in the vessel wall. These deranged processes culminate in an exuberant proliferative response that occludes the pulmonary arterial (PA) lumen and obliterates the most distal intraacinar vessels. Here, we describe emerging therapies based on preclinical studies that address these converging pathways.

Indexed as

AnimalsBone Morphogenetic Protein Receptors, Type IIEstrogensGlycolysisHumansHypertension, PulmonaryMutationPancreatic ElastaseReceptors, SerotoninSerotonin Plasma Membrane Transport ProteinsSignal TransductionStem CellsBMPR2 protein, humanBone Morphogenetic Protein Receptors, Type IIEstrogensPancreatic ElastaseReceptors, SerotoninSerotonin Plasma Membrane Transport Proteins

Identifiers

PMID23202738
PMCPMC3533531

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.