Evidence map›Paper›PMID 24913149›Full record

Trial reportJournal of biomedical science2014

Downregulation of Sirt1 as aging change in advanced heart failure.

Tse-Min Lu, Jia-Yun Tsai, Yen-Chung Chen, Chun-Yang Huang, Hung-Lung Hsu, Chi-Feng Weng, Chun-Che Shih, Chiao-Po Hsu

Open access · diamondAbstract readClinical Trial
In one paragraph

Trial report in Journal of biomedical science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

62 citing papers in PubMed, 109 citations in OpenAlex.

  1. Review
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  9. Acetylation in Cardiac Aging: Molecular Mechanism and Therapeutic Approaches.Results and problems in cell differentiation · 2025
    Review
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  12. Review
  13. Article
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  17. Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023
    Review
  18. Article
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  20. Review

2 more citing papers are in PubMed but not listed here.

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

8 authors at 4 institutions in 2 countries.

Tse-Min Lu
Jia-Yun Tsai
Yen-Chung Chen
Chun-Yang Huang
Hung-Lung Hsu
Chi-Feng Weng
Chun-Che Shih
Chiao-Po HsuNational Yang-Ming University, Institute of Clinical Medicine, School of Medicine, Taipei, Taiwan. chiaopo@ms39.hinet.net.
Taipei Veterans General Hospital · TWNational Yang Ming Chiao Tung University · TWMemorial Hospital of South Bend · USNational Yang Ming University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn congestive heart failure the balance between cell death and cell survival in cardiomyocytes is compromised. Sirtuin 1 (Sirt1) activates cell survival machinery and has been shown to be protective against ischemia/reperfusion injury in murine heart. The role of Sirt1 in heart failure, especially in human hearts is not clear.

resultsThe expression of Sirt1 and other (associated) downstream molecules in human cardiomyocytes from patients with advanced heart failure was examined. Sirt1 was down-regulated (54.92% ± 7.80% in advanced heart failure samples compared with healthy control cardiomyocytes). The modulation of molecules involved in cardiomyocyte survival and death in advanced heart failure were also examined. The expression of Mn-superoxide dismutase and thioredoxin1, as well as an antiapoptotic molecule, Bcl-xL, were all significantly reduced in advanced heart failure cardiomyoctes (0.71 ± 0.02-fold, 0.61 ± 0.05-fold, and 0.53 ± 0.08-fold vs. control, respectively); whereas the expression of proapoptotic molecule Bax was significantly increased (1.62 ± 0.18-fold vs. control). Increased TUNEL-positive number of cardiomyocytes and oxidative stress, confirmed by 8-hydorxydeoxyguanosine staining, were associated with advanced heart failure. The AMPK-Nampt-Sirt1 axis also showed inhibition in advanced heart failure in addition to severely impaired AMPK activation. Increased p53 (acetyl form) and decreased FoxO1 translocation in the nucleus may be the mechanism of down-regulation of antioxidants and up-regulation of proapoptotic molecules due to low expression of Sirt1.

conclusionIn advanced heart failure, low Sirt1 expression, like aging change may be a significant contributing factor in the downregulation of antioxidants and upregulation of proapoptotic molecules through the p53, FoxO1, and oxidative stress pathways.

Indexed as

Down-RegulationGene Expression Regulation, EnzymologicAgingAMP-Activated Protein KinasesAnimalsbcl-2-Associated X Proteinbcl-X ProteinCell DeathCell Line, TumorFemaleForkhead Box Protein O1Forkhead Transcription FactorsHeart FailureHumansMaleMyocytes, CardiacAMP-Activated Protein KinasesBAX protein, humanBax protein, ratbcl-2-Associated X ProteinBCL2L1 protein, humanBcl2l1 protein, ratbcl-X ProteinForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanFoxo1 protein, ratNerve Tissue ProteinsSIRT1 protein, humanSirt1 protein, ratSirtuin 1Superoxide DismutaseTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID24913149
PMCPMC4113120
OpenAlexW2133407146

What OpenQuestion holds

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LicenceCC BY
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.