Evidence map›Paper›PMID 23372926›Full record

ArticlePulmonary circulation2012

A process-based review of mouse models of pulmonary hypertension.

Mita Das, Joshua Fessel, Haiyang Tang, James West

Open access · bronzeAbstract read
In one paragraph

Article in Pulmonary circulation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Repetitive sulfur dioxide exposure in mice models post-deployment respiratory syndrome.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. A New "TYK" Tok Era for the Study of Long Noncoding RNAs in Pulmonary Hypertension.American journal of respiratory and critical care medicine · 2020
    Article
  8. Pulmonary Hypertension and ATP-Sensitive Potassium Channels.Hypertension (Dallas, Tex. : 1979) · 2019
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Purinergic dysregulation in pulmonary hypertension.American journal of physiology. Heart and circulatory physiology · 2016
    Article
  14. Pathogenic role of calcium-sensing receptors in the development and progression of pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  15. Review
  16. Article
  17. Article
  18. Article
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 3 institutions in 1 country.

Mita DasDepartment of Internal Medicine, University of Arkansas Medical Sciences, Little Rock, Arkansas, USA.
Joshua Fessel
Haiyang Tang
James West
Vanderbilt University Medical Center · USUniversity of Arkansas for Medical Sciences · USUniversity of Illinois Urbana-Champaign · US

Funding

Interventions Against the Molecular Etiology of BMPR2-induced PAHR01HL095797 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WEST, JAMES D · 2010 to 2022
$6.7M
NHLBI NIH HHS R01 HL095797
6 · The paper itself

Abstract

Genetically modified mouse models have unparalleled power to determine the mechanisms behind different processes involved in the molecular and physiologic etiology of various classes of human pulmonary hypertension (PH). Processes known to be involved in PH for which there are extensive mouse models available include the following: (1) Regulation of vascular tone through secreted vasoactive factors; (2) regulation of vascular tone through potassium and calcium channels; (3) regulation of vascular remodeling through alteration in metabolic processes, either through alteration in substrate usage or through circulating factors; (4) spontaneous vascular remodeling either before or after development of elevated pulmonary pressures; and (5) models in which changes in tone and remodeling are primarily driven by inflammation. PH development in mice is of necessity faster and with different physiologic ramifications than found in human disease, and so mice make poor models of natural history of PH. However, transgenic mouse models are a perfect tool for studying the processes involved in pulmonary vascular function and disease, and can effectively be used to test interventions designed against particular molecular pathways and processes involved in disease.

Indexed as

mouse modelspulmonary hypertensionvascular remodeling

Identifiers

PMID23372926
PMCPMC3555412
OpenAlexW2042155826

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.