Evidence map›Paper›PMID 26299964›Full record

ArticleCell reports2015

PGC-1α Modulates Telomere Function and DNA Damage in Protecting against Aging-Related Chronic Diseases.

Shiqin Xiong, Nikolay Patrushev, Farshad Forouzandeh, Lula Hilenski, R Wayne Alexander

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Unveiling the telomere-p53-PGC ageing axis.Nature reviews. Endocrinology · 2023
    Article
  12. Toxicology of pharmaceutical and nutritional longevity compounds.Expert reviews in molecular medicine · 2023
    Review
  13. Review
  14. Review
  15. Mitochondrial Dysfunction in the Cardio-Renal Axis.International journal of molecular sciences · 2023
    Review
  16. Article
  17. Role of angiotensin II in aging.Frontiers in aging neuroscience · 2022
    Review
  18. Article
  19. Mitochondria as a Cellular Hub in Infection and Inflammation.International journal of molecular sciences · 2021
    Review
  20. Multi-Omics Approach to Mitochondrial DNA Damage in Human Muscle Fibers.International journal of molecular sciences · 2021
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Shiqin XiongDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Nikolay PatrushevDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Farshad ForouzandehDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Lula HilenskiDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
R Wayne AlexanderDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA. Electronic address: ralexan@emory.edu.
Emory University · US

Funding

ANGIOTENSIN II RECEPTOR SIGNALING DOMAINSR01HL060728 · NHLBI · EMORY UNIVERSITY · PI ALEXANDER, ROBERT WAYNE · 1998 to 2010
$3.0M
NHLBI NIH HHS HHSN268201000043CNHLBI NIH HHS HL60728NHLBI NIH HHS R01 HL060728PHS HHS HHSN268201000043C
6 · The paper itself

Abstract

Cellular senescence and organismal aging predispose age-related chronic diseases, such as neurodegenerative, metabolic, and cardiovascular disorders. These diseases emerge coincidently from elevated oxidative/electrophilic stress, inflammation, mitochondrial dysfunction, DNA damage, and telomere dysfunction and shortening. Mechanistic linkages are incompletely understood. Here, we show that ablation of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) accelerates vascular aging and atherosclerosis, coinciding with telomere dysfunction and shortening and DNA damage. PGC-1α deletion reduces expression and activity of telomerase reverse transcriptase (TERT) and increases p53 levels. Ectopic expression of PGC-1α coactivates TERT transcription and reverses telomere malfunction and DNA damage. Furthermore, alpha lipoic acid (ALA), a non-dispensable mitochondrial cofactor, upregulates PGC-1α-dependent TERT and the cytoprotective Nrf-2-mediated antioxidant/electrophile-responsive element (ARE/ERE) signaling cascades, and counteracts high-fat-diet-induced, age-dependent arteriopathy. These results illustrate the pivotal importance of PGC-1α in ameliorating senescence, aging, and associated chronic diseases, and may inform novel therapeutic approaches involving electrophilic specificity.

Indexed as

DNA DamageTelomere ShorteningAnimalsAntioxidant Response ElementsAtherosclerosisBlood VesselsMiceMice, Inbred C57BLNF-E2-Related Factor 2Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaTelomeraseTelomereThioctic AcidTranscription FactorsTumor Suppressor Protein p53Nfe2l2 protein, mouseNF-E2-Related Factor 2Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseTelomeraseTert protein, mouseThioctic AcidTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID26299964
PMCPMC4549794
OpenAlexW1483238308

What OpenQuestion holds

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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.