Evidence map›Paper›PMID 23771884›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013

Id proteins are critical downstream effectors of BMP signaling in human pulmonary arterial smooth muscle cells.

Jun Yang, Xiaohui Li, Ying Li, Mark Southwood, Lingying Ye, Lu Long, Rafia S Al-Lamki, Nicholas W Morrell

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

64 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Article
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  4. The role of Id genes on pulmonary hypertension development in left heart failure.American heart journal plus : cardiology research and practice · 2026
    Article
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  8. Targeted delivery ofActa pharmaceutica Sinica. B · 2025
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4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Jun YangDept. of Medicine, Level 5, Box 157 Addenbrooke's Hospitals, Hills Rd., Cambridge, CB2 0QQ, UK.. nwm23@cam.ac.uk.
Xiaohui Li
Ying Li
Mark Southwood
Lingying Ye
Lu Long
Rafia S Al-Lamki
Nicholas W Morrell
Papworth Hospital · GBCentral South University · CNSecond Military Medical University · CNUniversity of Cambridge · GB

Funding

British Heart Foundation PG/06/149/21972British Heart Foundation RG/08/002/24718British Heart Foundation RG/13/4/30107Medical Research Council G0800784Medical Research Council G1000847
6 · The paper itself

Abstract

Bone morphogenetic protein type II receptor (BMPR-II) mutations are responsible for over 70% of cases of heritable pulmonary arterial hypertension (PAH). Loss of BMP signaling promotes pulmonary vascular remodeling via modulation of pulmonary artery smooth muscle cell (PASMC) proliferation. Id proteins (Id1-4) are major downstream transcriptional targets of BMP signaling. However, the impact of BMPR-II mutation on the expression of the range of Id proteins and the contribution of individual Id proteins to abnormal PASMC function remain unclear. Human PASMCs were used to determine the expression of Id proteins (Id1-4) by real-time PCR and immunoblotting. The BMP responses in control cells were compared with PASMCs harboring BMPR-II mutations and cells in which BMPR-II was knocked down by siRNA transfection. Id3 expression in pulmonary vessels was also investigated in BMPR-II mutant mice and in patients with heritable PAH. BMP4 and BMP6, but not BMP9, induced mRNA expression of Id1, Id2, and Id3. The BMP-stimulated induction of Id1 and Id3 was markedly reduced in BMPR-II mutant PASMCs and in control PASMCs following siRNA silencing of BMPR-II. Pulmonary arteries in BMPR-II mutant mice and patients with heritable PAH demonstrated reduced levels of Id3 compared with control subjects. Lentiviral overexpression of Id3 reduced cell cycle progression and inhibited proliferation of PASMCs. Lipopolysaccharide further reduced Id3 expression in mutant PASMCs. In conclusion, Id proteins, and particularly Id1 and Id3, are critical downstream effectors of BMP signaling in PASMCs. Loss of BMPR-II function reduces the induction of Id genes in PASMCs, Id1, and Id3 regulate the proliferation of PASMCs via cell cycle inhibition, an effect that may be exacerbated by inflammatory stimuli.

Indexed as

AnimalsBone Morphogenetic Protein Receptors, Type IIBone Morphogenetic ProteinsCell CycleCell ProliferationFamilial Primary Pulmonary HypertensionGene Expression RegulationHumansHypertension, PulmonaryInhibitor of Differentiation ProteinsLipopolysaccharidesLungMiceMice, Mutant StrainsMyocytes, Smooth MusclePulmonary ArteryBone Morphogenetic Protein Receptors, Type IIBone Morphogenetic ProteinsInhibitor of Differentiation ProteinsLipopolysaccharidesRNA, Messengerbone morphogenetic protein type II receptorcell cycleIdpulmonary arterial smooth muscle cellpulmonary hypertension

Identifiers

PMID23771884
PMCPMC3891012
OpenAlexW2157735464

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.