Evidence map›Paper›PMID 27591245›Full record

ReviewAmerican journal of physiology. Lung cellular and molecular physiology2016

Update on novel targets and potential treatment avenues in pulmonary hypertension.

John C Huetsch, Karthik Suresh, Meghan Bernier, Larissa A Shimoda

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Ginsenoside RbChinese herbal medicines · 2024
    Review
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  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Mitochondrial dysfunction and pulmonary hypertension: cause, effect, or both.American journal of physiology. Lung cellular and molecular physiology · 2018
    Review
  13. Article
  14. Article
  15. 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 1 institution in 1 country.

John C HuetschDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland; and.
Karthik SureshDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland; and.
Meghan BernierDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland.
Larissa A ShimodaDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland; and lshimod1@jhmi.edu.
Johns Hopkins University · US

Funding

Aquaporin 1 and pulmonary hypertensionR01HL126514 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SHIMODA, LARISSA A. · 2015 to 2025
$4.5M
Na+/H+ exchange in pulmonary hypertensionR01HL073859 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SHIMODA, LARISSA A. · 2003 to 2020
$4.2M
Institutional Training for PediatriciansT32HD044355 · NICHD · JOHNS HOPKINS UNIVERSITY · PI BRADY, TAMMY MCLOUGHLIN · 2003 to 2023
$4.1M
The Calpain/CaMKII/NHE Signaling Pathway in PAHK08HL133475 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI HUETSCH, JOHN · 2016 to 2019
$687k
NHE1 signaling in Pulmonary Arterial HypertensionF32HL124727 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI HUETSCH, JOHN · 2014 to 2015
$122k
Role of CD36 in ROS induced Ca influx in lung microvascular endothelial cellsF32HL124930 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SURESH, KARTHIK · 2014 to 2015
$116k
NHLBI NIH HHS F32 HL124727NHLBI NIH HHS F32 HL124930NHLBI NIH HHS K08 HL133475NHLBI NIH HHS R01 HL073859NHLBI NIH HHS R01 HL126514NICHD NIH HHS T32 HD044355
6 · The paper itself

Abstract

Pulmonary hypertension (PH) is a condition marked by a combination of constriction and remodeling within the pulmonary vasculature. It remains a disease without a cure, as current treatments were developed with a focus on vasodilatory properties but do not reverse the remodeling component. Numerous recent advances have been made in the understanding of cellular processes that drive pathologic remodeling in each layer of the vessel wall as well as the accompanying maladaptive changes in the right ventricle. In particular, the past few years have yielded much improved insight into the pathways that contribute to altered metabolism, mitochondrial function, and reactive oxygen species signaling and how these pathways promote the proproliferative, promigratory, and antiapoptotic phenotype of the vasculature during PH. Additionally, there have been significant advances in numerous other pathways linked to PH pathogenesis, such as sex hormones and perivascular inflammation. Novel insights into cellular pathology have suggested new avenues for the development of both biomarkers and therapies that will hopefully bring us closer to the elusive goal: a therapy leading to reversal of disease.

Indexed as

Molecular Targeted TherapyAnimalsBiomarkersDisease Models, AnimalHumansHypertension, PulmonaryModels, BiologicalSignal TransductionBiomarkerspulmonary arterial hypertensionremodelingvascular

Identifiers

PMID27591245
PMCPMC5130539
OpenAlexW2518556995

What Socratic 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 Socratic graph.