Evidence map›Paper›PMID 18765277›Full record

ArticleExperimental gerontology2008

Renin-angiotensin system inhibitors protect against age-related changes in rat liver mitochondrial DNA content and gene expression.

Elena M V de Cavanagh, Idhaliz Flores, Marcelo Ferder, Felipe Inserra, León Ferder

Open access · greenAbstract read
In one paragraph

Article in Experimental gerontology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. The role of angiotensin II in nonalcoholic steatohepatitis.Molecular and cellular endocrinology · 2013
    Review
  8. Article
  9. Article
  10. Angiotensin inhibition and longevity: a question of hydration.Pflugers Archiv : European journal of physiology · 2011
    Review
  11. Angiotensin II blockade upregulates the expression of Klotho, the anti-ageing gene, in an experimental model of chronic cyclosporine nephropathy.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2011
    Article
  12. Review
  13. Angiotensin receptors as determinants of life span.Pflugers Archiv : European journal of physiology · 2010
    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 2 institutions in 2 countries.

Elena M V de CavanaghInstitute of Cardiovascular Pathophysiology (INFICA), School of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
Idhaliz Flores
Marcelo Ferder
Felipe Inserra
León Ferder
Ponce Health Sciences University · PRUniversity of Buenos Aires · AR

Funding

VIRAL SEQUENCES IN PEDIATRIC HIV INFECTION IN PRG12RR003050 · NCRR · PONCE SCHOOL OF MEDICINE · PI ARMSTRONG, RAUL A · 1985 to 2011
$28.1M
NCRR NIH HHS G12 RR003050NCRR NIH HHS G12RR03050
6 · The paper itself

Abstract

Chronic renin-angiotensin system inhibition protects against liver fibrosis, ameliorates age-associated mitochondrial dysfunction and increases rodent lifespan. We hypothesized that life-long angiotensin-II-mediated stimulation of oxidant generation might participate in mitochondrial DNA "common deletion" formation, and the resulting impairment of bioenergetic capacity. Enalapril (10 mg/kg/d) or losartan (30 mg/kg/d) administered during 16.5 months were unable to prevent the age-dependent accumulation of rat liver mitochondrial DNA "common deletion", but attenuated the decrease of mitochondrial DNA content. This evidence - together with the enhancement of NRF-1 and PGC-1 mRNA contents - seems to explain why enalapril and losartan improved mitochondrial functioning and lowered oxidant production, since both the absolute number of mtDNA molecules and increased NRF-1 and PGC-1 transcription are positively related to mitochondrial respiratory capacity, and PGC-1 protects against increases in ROS production and damage. Oxidative stress evoked by abnormal respiratory function contributes to the pathophysiology of mitochondrial disease and human aging. If the present mitochondrial actions of renin-angiotensin system inhibitors are confirmed in humans they may modify the therapeutic significance of that strategy.

Indexed as

AgingAnimalsDNA, MitochondrialGene ExpressionMaleMitochondriaMitochondrial DiseasesOxidative StressRatsRats, WistarReactive Oxygen SpeciesRenin-Angiotensin SystemDNA, MitochondrialReactive Oxygen Species

Identifiers

PMID18765277
PMCPMC4871262
OpenAlexW2052813773

What OpenQuestion holds

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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.