Evidence map›Paper›PMID 29513568›Full record

ArticleAmerican journal of physiology. Cell physiology2018

Overexpression of hexokinase 2 reduces mitochondrial calcium overload in coronary endothelial cells of type 2 diabetic mice.

Minglin Pan, Ying Han, Aninda Basu, Anzhi Dai, Rui Si, Conor Willson, Angela Balistrieri, Brian T Scott, Ayako Makino

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

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  6. CircRNA-miRNA interactions in atherogenesis.Molecular and cellular biochemistry · 2022
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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

9 authors at 4 institutions in 2 countries.

Minglin PanDepartment of Medicine, University of Illinois at Chicago , Chicago, Illinois.
Ying HanDepartment of Physiology, University of Arizona , Tucson, Arizona.
Aninda BasuDepartment of Medicine, University of Illinois at Chicago , Chicago, Illinois.
Anzhi DaiDepartment of Medicine, University of Illinois at Chicago , Chicago, Illinois.
Rui SiDepartment of Physiology, University of Arizona , Tucson, Arizona.
Conor WillsonDepartment of Physiology, University of Arizona , Tucson, Arizona.
Angela BalistrieriDepartment of Physiology, University of Arizona , Tucson, Arizona.
Brian T ScottDepartment of Medicine, University of California, San Diego, La Jolla, California.
Ayako MakinoDepartment of Physiology, University of Arizona , Tucson, Arizona.
University of Arizona · USUniversity of Illinois Chicago · USUniversity of California, San Diego · USSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

Coronary Endothelial Cell Dysfunction in Diabetes: Role of MFGE8R01HL142214 · NHLBI · UNIVERSITY OF FLORIDA · PI Yun Sok Lee, Ayako Makino · 2018 to 2026
$3.2M
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 HL142214
6 · The paper itself

Abstract

Coronary microvascular rarefaction, due to endothelial cell (EC) dysfunction, is one of the causes of increased morbidity and mortality in diabetes. Coronary ECs in diabetes are more apoptotic due partly to mitochondrial calcium overload. This study was designed to investigate the role of hexokinase 2 (HK2, an endogenous inhibitor of voltage-dependent anion channel) in coronary endothelial dysfunction in type 2 diabetes. We used mouse coronary ECs (MCECs) isolated from type 2 diabetic mice and human coronary ECs (HCECs) from type 2 diabetic patients to examine protein levels and mitochondrial function. ECs were more apoptotic and capillary density was lower in the left ventricle of diabetic mice than the control. MCECs from diabetic mice exhibited significant increase in mitochondrial Ca

Indexed as

AnimalsApoptosisBlood GlucoseCalciumCoronary VesselsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diabetic AngiopathiesEndothelial CellsHexokinaseHumansMaleMice, Inbred C57BLMitochondriaReactive Oxygen SpeciesUbiquitinationBlood GlucoseCalciumHexokinasehexokinase 2, mouseHK2 protein, humanReactive Oxygen SpeciesHK2mitochondrial Ca2+ overloadROS

Identifiers

PMID29513568
PMCPMC6334999
OpenAlexW2791888854

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.