Evidence map›Paper›PMID 22245772›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2012

New mechanisms of pulmonary arterial hypertension: role of Ca²⁺ signaling.

Frank K Kuhr, Kimberly A Smith, Michael Y Song, Irena Levitan, Jason X-J Yuan

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

102 citing papers in PubMed, 177 citations in OpenAlex.

  1. Review
  2. Variation inCirculation research · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Growth factors involved in vascular remodeling in pulmonary arterial hypertension.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2025
    Review
  10. Article
  11. Up-regulated expression of two-pore domain KFrontiers in cardiovascular medicine · 2024
    Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

42 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

5 authors at 1 institution in 1 country.

Frank K KuhrSection of Pulmonary, Critical Care, Sleep, and Allergy, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612, USA.
Kimberly A Smith
Michael Y Song
Irena Levitan
Jason X-J Yuan
University of Illinois Chicago · US

Funding

Therapeutic Potential of FTY720 Analogues in Lung InjuryP01HL098050 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI NATARAJAN, VISWANATHAN · 2011 to 2015
$10.9M
Systems Biology CoreP01HL098053 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI POWELL, FRANK L. · 2010 to 2014
$10.2M
Training Grant in GastroenterologyT32DK007202 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GHOSH, PRADIPTA · 1985 to 2022
$7.7M
Cholesterol Regulation of Endothelial K+ ChannelsR01HL073965 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI LEVITAN, IRENA · 2004 to 2024
$7.3M
Impact of dyslipidemia on endothelial biomechanicsR01HL083298 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LEVITAN, IRENA, MINSHALL, RICHARD D · 2007 to 2021
$7.0M
Capacitative Ca2+ Entry in Pulmonary Myocyte GrowthR01HL066012 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI YUAN, JASON X J · 2002 to 2016
$5.2M
NHLBI NIH HHS P01-HL-098050NHLBI NIH HHS P01-HL-098053NHLBI NIH HHS R01 HL066012NHLBI NIH HHS R01-HL-066012NHLBI NIH HHS R01 HL073965NHLBI NIH HHS R01 HL083298NIDDK NIH HHS T32 DK007202
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a severe and progressive disease that usually culminates in right heart failure and death if left untreated. Although there have been substantial improvements in our understanding and significant advances in the management of this disease, there is a grim prognosis for patients in the advanced stages of PAH. A major cause of PAH is increased pulmonary vascular resistance, which results from sustained vasoconstriction, excessive pulmonary vascular remodeling, in situ thrombosis, and increased pulmonary vascular stiffness. In addition to other signal transduction pathways, Ca(2+) signaling in pulmonary artery smooth muscle cells (PASMCs) plays a central role in the development and progression of PAH because of its involvement in both vasoconstriction, through its pivotal effect of PASMC contraction, and vascular remodeling, through its stimulatory effect on PASMC proliferation. Altered expression, function, and regulation of ion channels and transporters in PASMCs contribute to an increased cytosolic Ca(2+) concentration and enhanced Ca(2+) signaling in patients with PAH. This review will focus on the potential pathogenic role of Ca(2+) mobilization, regulation, and signaling in the development and progression of PAH.

Indexed as

AnimalsApoptosisCalciumCalcium ChannelsCalcium SignalingCarrier ProteinsCaveolaeCaveolinsCell ProliferationHomeodomain ProteinsHumansHypertension, PulmonaryMyocytes, Smooth MusclePotassium ChannelsSuppressor of Cytokine Signaling ProteinsTransient Receptor Potential ChannelsCalciumCalcium ChannelsCarrier ProteinsCaveolinsHomeodomain ProteinsPotassium ChannelsRBX1 protein, humanSuppressor of Cytokine Signaling ProteinsTLX2 protein, humanTransient Receptor Potential Channels

Identifiers

PMID22245772
PMCPMC3330808
OpenAlexW1999887461

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.