Evidence map›Paper›PMID 18202313›Full record

ArticleCirculation research2008

Activation of cardiac progenitor cells reverses the failing heart senescent phenotype and prolongs lifespan.

Arantxa Gonzalez, Marcello Rota, Daria Nurzynska, Yu Misao, Jochen Tillmanns, Caroline Ojaimi, M Elena Padin-Iruegas, Patrick Müller, Grazia Esposito, Claudia Bearzi and 11 more

RetractedOpen access · bronzeAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Circulation research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
13.1field-weighted citation impact, top 1% 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

83 citing papers in PubMed, 182 citations in OpenAlex.

  1. Review
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  15. Article
  16. The Aging Heart.Cold Spring Harbor perspectives in medicine · 2015
    Review
  17. Cardiac aging - Getting to the stem of the problem.Journal of molecular and cellular cardiology · 2015
    Review
  18. Article
  19. Review
  20. Cardiac stem cells: biology and clinical applications.Antioxidants & redox signaling · 2014
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 1 institution in 1 country.

Arantxa GonzalezDepartment of Anesthesia, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Marcello Rota
Daria Nurzynska
Yu Misao
Jochen Tillmanns
Caroline Ojaimi
M Elena Padin-Iruegas
Patrick Müller
Grazia Esposito
Claudia Bearzi
Serena Vitale
Buddhadeb Dawn
Santosh K Sanganalmath
Mathue Baker
Thomas H Hintze
Roberto Bolli
Konrad Urbanek
Toru Hosoda
Piero Anversa
Jan Kajstura
Annarosa Leri
New York Medical College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure is the leading cause of death in the elderly, but whether this is the result of a primary aging myopathy dictated by depletion of the cardiac progenitor cell (CPC) pool is unknown. Similarly, whether current lifespan reflects the ineluctable genetic clock or heart failure interferes with the genetically determined fate of the organ and organism is an important question. We have identified that chronological age leads to telomeric shortening in CPCs, which by necessity generate a differentiated progeny that rapidly acquires the senescent phenotype conditioning organ aging. CPC aging is mediated by attenuation of the insulin-like growth factor-1/insulin-like growth factor-1 receptor and hepatocyte growth factor/c-Met systems, which do not counteract any longer the CPC renin-angiotensin system, resulting in cellular senescence, growth arrest, and apoptosis. However, pulse-chase 5-bromodeoxyuridine-labeling assay revealed that the senescent heart contains functionally competent CPCs that have the properties of stem cells. This subset of telomerase-competent CPCs have long telomeres and, following activation, migrate to the regions of damage, where they generate a population of young cardiomyocytes, reversing partly the aging myopathy. The senescent heart phenotype and heart failure are corrected to some extent, leading to prolongation of maximum lifespan.

Indexed as

Adult Stem CellsAgingAnimalsAntigens, DifferentiationApoptosisCell CountCell DifferentiationCell DivisionCell MovementCellular SenescenceCyclin-Dependent Kinase Inhibitor p16Disease Models, AnimalDrug Administration RoutesHeartHeart FailureHepatocyte Growth FactorAntigens, DifferentiationCyclin-Dependent Kinase Inhibitor p16Hepatocyte Growth FactorInsulin-Like Growth Factor IReceptors, Growth Factor

Identifiers

PMID18202313
OpenAlexW2163555597

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.