Evidence map›Paper›PMID 23430128›Full record

ReviewHeart failure reviews2014

Reactive carbonyl species and their roles in sarcoplasmic reticulum Ca2+ cycling defect in the diabetic heart.

Chengju Tian, Fadhel Alomar, Caronda J Moore, Chun Hong Shao, Shelby Kutty, Jaipaul Singh, Keshore R Bidasee

Open access · greenAbstract readReview
In one paragraph

Review in Heart failure reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Glycation in the cardiomyocyte.Vitamins and hormones · 2024
    Review
  4. Metabolite signaling in the heart.Nature cardiovascular research · 2023
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Mitochondrial NADAntioxidants & redox signaling · 2019
    Review
  14. Article
  15. Review
  16. 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 5 institutions in 3 countries.

Chengju TianDepartments of Pharmacology and Experimental Neuroscience, Durham Research Center, University of Nebraska Medical Center, DRC 3047, Omaha, NE, 68198-5800, USA.
Fadhel Alomar
Caronda J Moore
Chun Hong Shao
Shelby Kutty
Jaipaul Singh
Keshore R Bidasee
University of Nebraska Medical Center · USCHI Health Creighton University Medical Center - Bergan Mercy · USDammam Central Hospital · SAUniversity of Central Lancashire · GBUniversity of Nebraska–Lincoln · US

Funding

Role of Ryanodine Receptors in Diabetic CadiomyopathyR01HL085061 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BIDASEE, KESHORE R · 2007 to 2010
$1.6M
NHLBI NIH HHS HL085061NHLBI NIH HHS R01 HL085061
6 · The paper itself

Abstract

Efficient and rhythmic cardiac contractions depend critically on the adequate and synchronized release of Ca(2+) from the sarcoplasmic reticulum (SR) via ryanodine receptor Ca(2+) release channels (RyR2) and its reuptake via sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA2a). It is well established that this orchestrated process becomes compromised in diabetes. What remain incompletely defined are the molecular mechanisms responsible for the dysregulation of RyR2 and SERCA2a in diabetes. Earlier, we found elevated levels of carbonyl adducts on RyR2 and SERCA2a isolated from hearts of type 1 diabetic rats and showed the presence of these posttranslational modifications compromised their functions. We also showed that these mono- and di-carbonyl reactive carbonyl species (RCS) do not indiscriminately react with all basic amino acid residues on RyR2 and SERCA2a; some residues are more susceptible to carbonylation (modification by RCS) than others. A key unresolved question in the field is which of the many RCS that are upregulated in the heart in diabetes chemically react with RyR2 and SERCA2a? This brief review introduces readers to the field of RCS and their roles in perturbing SR Ca(2+) cycling in diabetes. It also provides new experimental evidence that not all RCS that are upregulated in the heart in diabetes chemically react with RyR2 and SERCA2a, methylglyoxal and glyoxal preferentially do.

Indexed as

Diabetic CardiomyopathiesAnimalsHumansMyocardial ContractionMyocardiumProtein CarbonylationRyanodine Receptor Calcium Release ChannelSarcoplasmic Reticulum Calcium-Transporting ATPasesRyanodine Receptor Calcium Release ChannelSarcoplasmic Reticulum Calcium-Transporting ATPases

Identifiers

PMID23430128
PMCPMC4732283
OpenAlexW2013146358

What OpenQuestion holds

Textmetadata
LicenceTDM
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.