Evidence map›Paper›PMID 23737167›Full record

ReviewComprehensive Physiology2011

Pulmonary vascular disease related to hemodynamic stress in the pulmonary circulation.

Stephen Y Chan, Joseph Loscalzo

Open access · greenAbstract readReview
In one paragraph

Review in Comprehensive Physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Murine Aortopulmonary Shunt Model of Flow-Driven Pulmonary Hypertension-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  2. Article
  3. QuantitativeScientific reports · 2020
    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

2 authors at 2 institutions in 1 country.

Stephen Y ChanDivision of Cardiology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Joseph Loscalzo
Harvard University · USMassachusetts General Hospital · US

Funding

Redox regulation in Endothelial Progenitor CellsP01HL081587 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2005 to 2015
$21.5M
MULTIDISCIPLINARY RESEARCH TRAINING IN CARDIOLOGYT32HL007208 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI Patrick Thomas Ellinor, David E Sosnovik · 1985 to 2026
$16.1M
GPx-3 and Peroxide Flux in the Endothelial CellR37HL061795 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LOSCALZO, JOSEPH · 2007 to 2016
$4.3M
NHLBI PROTEOMICS INITIATIVEN01HV28178 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · 2007 to 2008
$2.8M
HOMOCYST(E)INE, OXIDATIVE STRESS, AND NITRIC OXIDER01HL058976 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LOSCALZO, JOSEPH · 1997 to 2004
$1.6M
PLATELET DERIVED REACTIVE OXYGEN SPECIES AND PLAQUER01HL061795 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LOSCALZO, JOSEPH · 1998 to 2006
$1.6M
Functions of the Hypoxia-Induced MicroRNA-210 in Pulmonary Vascular EndotheliumK08HL096834 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI CHAN, STEPHEN Y · 2010 to 2014
$687k
STRUCTURAL CHARACTERIZATION OF THE APOPROTEIN E RECEPTORR01HL028178 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI INNERARITY, THOMAS L. · 1986 to 1988
–
NHLBI PROTEOMICS INITIATIVE-N01HV28178N01HV028178 · HV · BOSTON UNIVERSITY MEDICAL CAMPUS · PI COSTELLO, CATHERINE E. · 2002 to 2006
–
NHLBI NIH HHS 5T32HL007208-30NHLBI NIH HHS HL 61795NHLBI NIH HHS K08 HL096834NHLBI NIH HHS N01 HV028178NHLBI NIH HHS N01 HV28178NHLBI NIH HHS P01 HL081587NHLBI NIH HHS R01 HL058976NHLBI NIH HHS R01 HL061795NHLBI NIH HHS R37 HL061795NHLBI NIH HHS T32 HL007208PHS HHS P01 81587
6 · The paper itself

Abstract

Hemodynamic stress in the pulmonary vessel is directly linked to the development of vascular remodeling and dysfunction, ultimately leading to pulmonary hypertension. Recently, some advances have been made in our molecular understanding of the exogenous upstream stimuli that initiate hemodynamic pertubations as well as the downstream vasoactive effectors that control these responses. However, much still remains unknown regarding how these complex signaling pathways connect in order to result in these characteristic pathophysiological changes. This chapter will describe our current understanding of and needed areas of research into the clinical, physiological, and molecular changes associated with pressure/volume overload in the pulmonary circulation.

Indexed as

AnimalsBlood PressureDisease Models, AnimalGenetic Predisposition to DiseaseHemodynamicsHumansHypertension, PulmonaryMechanotransduction, CellularPulmonary CirculationStress, Physiological

Identifiers

PMID23737167
PMCPMC3730284
OpenAlexW1692893177

What OpenQuestion holds

Textmetadata
LicenceTDM
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.