Evidence map›Paper›PMID 17250874›Full record

ArticleMechanisms of ageing and development2007

Cardiac overexpression of antioxidant catalase attenuates aging-induced cardiomyocyte relaxation dysfunction.

Jun Ren, Qun Li, Shan Wu, Shi-Yan Li, Sara A Babcock

Abstract read
In one paragraph

Article in Mechanisms of ageing and development, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Review
  3. Knockout of ACE-N facilitates improved cardiac function after myocardial infarction.Journal of molecular and cellular cardiology plus · 2023
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. The little big genome: the organization of mitochondrial DNA.Frontiers in bioscience (Landmark edition) · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Redox control of cardiac excitability.Antioxidants & redox signaling · 2013
    Review
  19. Review
  20. Review
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

5 authors at 1 institution in 1 country.

Jun RenDivision of Pharmaceutical Sciences & Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, WY 82071-2000, United States. jren@uwyo.edu
Qun Li
Shan Wu
Shi-Yan Li
Sara A Babcock
University of Wyoming · US

Funding

Role of Acetaldehyde in Alcoholic CardiomyopathyR01AA013412 · NIAAA · UNIVERSITY OF WYOMING · PI REN, JUN · 2004 to 2008
$1.0M
Antioxidant Transgenenes Alcoholic CardiomyopathyR15AA013575 · NIAAA · UNIVERSITY OF WYOMING · PI REN, JUN · 2002 to 2002
$141k
IGF-1, Oxidative Stress and Cardiovascular AgingR03AG021324 · NIA · UNIVERSITY OF WYOMING · PI REN, JUN · 2002 to 2002
$70k
NIAAA NIH HHS 1R15 AA13575-01NIAAA NIH HHS R01 AA013412NIAAA NIH HHS R15 AA013575NIA NIH HHS 1R03 AG21324-01NIA NIH HHS R03 AG021324
6 · The paper itself

Abstract

Catalase, an enzyme which detoxifies H2O2, may interfere with cardiac aging. To test this hypothesis, contractile and intracellular Ca2+ properties were evaluated in cardiomyocytes from young (3-4 months) and old (26-28 months) FVB and transgenic mice with cardiac overexpression of catalase. Contractile indices analyzed included peak shortening (PS), time-to-90% PS (TPS90), time-to-90% relengthening (TR90), half-width duration (HWD), maximal velocity of shortening/relengthening (+/-dL/dt) and intracellular Ca2+ levels or decay rate. Levels of advanced glycation endproduct (AGE), Na+/Ca2+ exchanger (NCX), sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2a), phospholamban (PLB), myosin heavy chain (MHC), membrane Ca2+ and K+ channels were measured by western blot. Catalase transgene prolonged survival while did not alter myocyte function by itself. Aging depressed+/-dL/dt, prolonged HWD, TR90 and intracellular Ca2+ decay without affecting other indices in FVB myocytes. Aged FVB myocytes exhibited a stepper decline in PS in response to elevated stimulus or a dampened rise in PS in response to elevated extracellular Ca2+ levels. Interestingly, aging-induced defects were nullified or significantly attenuated by catalase. AGE level was elevated by 5-fold in aged FVB compared with young FVB mice, which was reduced by catalase. Expression of SERCA2a, NCX and Kv1.2 K+ channel was significantly reduced although levels of PLB, L-type Ca2+ channel dihydropyridine receptor and beta-MHC isozyme remained unchanged in aged FVB hearts. Catalase restored NCX and Kv1.2 K+ channel but not SERCA2a level in aged mice. In summary, our data suggested that catalase protects cardiomyocytes from aging-induced contractile defect possibly via improved intracellular Ca2+ handling.

Indexed as

AgingAnimalsAntioxidantsBlotting, WesternCalcium-Binding ProteinsCalcium Channels, L-TypeCalcium SignalingCardiomyopathiesCatalaseElectrophoresis, Polyacrylamide GelGlycation End Products, AdvancedIsoenzymesMiceMice, TransgenicMyocardial ContractionMyocardiumAntioxidantsCalcium-Binding ProteinsCalcium Channels, L-TypeCatalaseGlycation End Products, AdvancedIsoenzymesMyosin Heavy ChainsPhospholambanPotassium ChannelsSarcoplasmic Reticulum Calcium-Transporting ATPasesSodium-Calcium Exchanger

Identifiers

PMID17250874
PMCPMC1847331
OpenAlexW2138406323

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.