Evidence map›Paper›PMID 19419974›Full record

ArticleHuman molecular genetics2009

Defective pulmonary vascular remodeling in Smad8 mutant mice.

Zheng Huang, Degang Wang, Kaori Ihida-Stansbury, Peter Lloyd Jones, James F Martin

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
5.7field-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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Defining the clinical validity of genes reported to cause pulmonary arterial hypertension.Genetics in medicine : official journal of the American College of Medical Genetics · 2023
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. The BMP Pathway in Blood Vessel and Lymphatic Vessel Biology.International journal of molecular sciences · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. A Rare Mutation in SMAD9 Associated With High Bone Mass Identifies the SMAD-Dependent BMP Signaling Pathway as a Potential Anabolic Target for Osteoporosis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020
    Article
  18. Article
  19. Molecular Research in Chronic Thromboembolic Pulmonary Hypertension.International journal of molecular sciences · 2019
    Review
  20. 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

5 authors at 2 institutions in 1 country.

Zheng HuangInstitute of Biosciences and Technology, Texas A&M System Health Science Center, 2121 W. Holcombe Blvd, Houston, TX 77030, USA.
Degang Wang
Kaori Ihida-Stansbury
Peter Lloyd Jones
James F Martin
Texas A&M University System · USUniversity of Pennsylvania · US

Funding

BMP SIGNALING IN CRANIOFACIAL DEVELOPMENTR01DE012324 · NIDCR · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI MARTIN, JAMES F · 2002 to 2012
$3.2M
PITX2 AND WNT'S IN CRANIOFACIAL DEVELOPMENTR01DE016329 · NIDCR · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI MARTIN, JAMES F · 2005 to 2008
$1.3M
NIDCR NIH HHS 2R01DE/HD12324-12NIDCR NIH HHS R01 DE016329NIDCR NIH HHS R01DE16329
6 · The paper itself

Abstract

Pulmonary artery hypertension (PAH), a progressive, lethal condition that results in pathologic changes in the pulmonary arterial tree, eventually leads to right heart failure. Work identifying mutations in the Type II Bone morphogenetic protein (Bmp) receptor, BmpRII, in families with PAH has implicated Bmp-signaling in the pathogenesis of PAH. However, the effectors downstream of BmpRII in PAH remain unclear since BmpRII signals via Smad-dependent and independent mechanisms. We investigated Smad8 function, a divergent receptor regulated Smad downstream of Bmp-signaling, using gene targeting in mice. We show that Smad8 loss of function in adults resulted in characteristic changes in distal pulmonary arteries including medial thickening and smooth muscle hyperplasia that is observed in patients with PAH. Smad8 mutant pulmonary vasculature had upregulated Activin/Tgfbeta signaling and pathologic remodeling with aberrant Prx1 and Tenascin-C expression. A subset of Smad8 mutants had pulmonary adenomas uncovering a function for Smad8 in normal growth control. These findings implicate Smad8 in both pulmonary hypertension and lung tumorigenesis and support Smad8 as a candidate gene for PAH in humans.

Indexed as

MutationAnimalsBone Morphogenetic ProteinsDisease Models, AnimalFemaleHumansHypertension, PulmonaryMaleMiceMice, KnockoutPulmonary ArterySignal TransductionSmad8 ProteinBone Morphogenetic ProteinsSmad8 Protein

Identifiers

PMID19419974
PMCPMC2706683
OpenAlexW2165770440

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.