Evidence map›Paper›PMID 28680577›Full record

ArticlePulmonary circulation2017

Hypoxia-induced pulmonary hypertension in type 2 diabetic mice.

Minglin Pan, Ying Han, Rui Si, Rui Guo, Ankit Desai, Ayako Makino

Open access · bronzeAbstract read
In one paragraph

Article in Pulmonary circulation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Mechanisms Underlying Altitude-Induced and Group 3 Pulmonary Hypertension.International journal of molecular sciences · 2026
    Review
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  16. Comparison of Pulmonary and Systemic NO- and PGIOxidative medicine and cellular longevity · 2018
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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

6 authors at 3 institutions in 2 countries.

Minglin PanDepartment of Medicine, University of Illinois at Chicago, Chicago, IL, USA.
Ying HanDepartment of Medicine, University of Illinois at Chicago, Chicago, IL, USA.
Rui SiDepartment of Physiology, University of Arizona, Tucson, AZ, USA.
Rui GuoDepartment of Physiology, University of Arizona, Tucson, AZ, USA.
Ankit DesaiDepartment of Medicine, University of Illinois at Chicago, Chicago, IL, USA.
Ayako MakinoDepartment of Medicine, University of Illinois at Chicago, Chicago, IL, USA.
University of Arizona · USUniversity of Illinois Chicago · USSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

Pathogenic Role of IL-18 in Sickle Cell Cardiomyopathy and Inducible Ventricular TachycardiaR01HL136603 · NHLBI · UNIVERSITY OF ARIZONA · PI DESAI, ANKIT A · 2017 to 2021
$2.4M
Cellular and Molecular Mechanisms of Coronary Endothelial Dysfunction in DiabetesR01HL115578 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MAKINO, AYAKO · 2012 to 2015
$1.5M
NHLBI NIH HHS R01 HL115578NHLBI NIH HHS R01 HL136603
6 · The paper itself

Abstract

Hypoxia-induced pulmonary hypertension (HPH) is a progressive disease that is mainly caused by chronic exposure to high altitude, chronic obstructive lung disease, and obstructive sleep apnea. The increased pulmonary vascular resistance and increased pulmonary arterial pressure result in increased right ventricular afterload, leading to right heart failure and increased morbidity. There are several clinical reports suggesting a link between PH and diabetes, insulin resistance, or obesity; however, it is unclear whether HPH is associated with diabetes as a progressive complication in diabetes. The major goal of this study is to examine the effect of diabetic "preconditioning" or priming effect on the progression of HPH and define the molecular mechanisms that explain the link between diabetes and HPH. Our data show that HPH is significantly enhanced in diabetic mice, while endothelium-dependent relaxation in pulmonary arteries is significantly attenuated in chronically hypoxic diabetic mice (DH). In addition, we demonstrate that mouse pulmonary endothelial cells (MPECs) isolated from DH mice exhibit a significant increase in mitochondrial reactive oxygen species (ROS) concentration and decreased SOD2 protein expression. Finally, scavenging mitochondrial ROS by mitoTempol restores endothelium-dependent relaxation in pulmonary arteries that is attenuated in DH mice. These data suggest that excessive mitochondrial ROS production in diabetic MPECs leads to the development of severe HPH in diabetic mice exposed to hypoxia.

Indexed as

endothelial cellendothelium-dependent relaxationmitochondriapulmonary arteryreactive oxygen species (ROS)

Identifiers

PMID28680577
PMCPMC5448524
OpenAlexW2552383643

What OpenQuestion holds

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LicenceCC BY-NC
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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.