Evidence map›Paper›PMID 20573996›Full record

ArticleAmerican journal of physiology. Cell physiology2010

Cardiac contractile dysfunction during acute hyperglycemia due to impairment of SERCA by polyol pathway-mediated oxidative stress.

Wai Ho Tang, Wing Tim Cheng, Gennadi M Kravtsov, Xiao Yong Tong, Xiu Yun Hou, Sookja K Chung, Stephen Sum Man Chung

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 83 citations in OpenAlex.

  1. Trial
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  11. Carvacrol protects the ARPE19 retinal pigment epithelial cells against high glucose-induced oxidative stress, apoptosis, and inflammation by suppressing the TRPM2 channel signaling pathways.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022
    Article
  12. CaPflugers Archiv : European journal of physiology · 2022
    Review
  13. PERM1 regulates energy metabolism in the heartFrontiers in cardiovascular medicine · 2022
    Article
  14. Article
  15. Article
  16. Fructose Metabolism and Cardiac Metabolic Stress.Frontiers in pharmacology · 2021
    Review
  17. Review
  18. Glucose Metabolism in Cardiac Hypertrophy and Heart Failure.Journal of the American Heart Association · 2019
    Review
  19. Article
  20. 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

7 authors at 3 institutions in 2 countries.

Wai Ho TangDepartment of Physiology, Faculty of Medicine, University of Hong Kong, Hong Kong, China.
Wing Tim Cheng
Gennadi M Kravtsov
Xiao Yong Tong
Xiu Yun Hou
Sookja K Chung
Stephen Sum Man Chung
Chinese University of Hong Kong · HKBoston University · USUniversity of Hong Kong · HK

Funding

Redox Regulation of SERCA by Nitric OxideR01HL031607 · NHLBI · BOSTON UNIVERSITY MEDICAL CENTER HOSP · PI COHEN, RICHARD A · 1985 to 2013
$4.8M
NHLBI NIH HHS R01 HL031607NHLBI NIH HHS R01-HL-31607-25
6 · The paper itself

Abstract

Hyperglycemia is an indication of poor outcome for heart attack patients, even for nondiabetic patients with stress-induced hyperglycemia. Previous studies showed that inhibition of aldose reductase, the first and rate-limiting enzyme of the polyol pathway, attenuated contractile dysfunction in diabetic animals, but the mechanism is unclear. We therefore wanted to find out whether the polyol pathway also contributes to acute hyperglycemia-induced cardiac contractile dysfunction, and determine the mechanism involved. Rat hearts were isolated and retrogradely perfused with Krebs buffer containing either normal or high concentrations of glucose for 2 h. Short exposure to high-glucose medium led to contractile dysfunction as indicated by decreased -dP/dt(max), as well as elevation in left ventricular end-diastolic pressure. Cardiomyocytes incubated in high-glucose medium showed abnormal Ca2+ signaling, most likely because of decreased activity of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) inactivated by oxidative stress. Inhibition of aldose reductase or sorbitol dehydrogenase, the second enzyme in the polyol pathway, ameliorated contractile dysfunction, attenuated oxidative stress, and normalized Ca2+ signaling and SERCA activity caused by high glucose, indicating that the polyol pathway is the major contributor to acute hyperglycemia-induced oxidative stress leading to the inactivation of SERCA and contractile dysfunction.

Indexed as

Oxidative StressSignal TransductionAcute DiseaseAldehyde ReductaseAnimalsCalcium SignalingGlucoseGlutathioneHeartHyperglycemiaIn Vitro TechniquesLactic AcidMaleMyocardial ContractionMyocardiumOxidation-ReductionAldehyde ReductaseAtp2a2 protein, ratGlucoseGlutathioneLactic AcidPeroxynitrous AcidPyruvic AcidSarcoplasmic Reticulum Calcium-Transporting ATPasesSuperoxidesTyrosine

Identifiers

PMID20573996
PMCPMC2944313
OpenAlexW1978779225

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.