Evidence map›Paper›PMID 11790923›Full record

ReviewHeart failure reviews2002

Acute and chronic adaptation to hemodynamic overload and ischemia in the aged heart.

Shogen Isoyama, Yuko Nitta-Komatsubara

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Observational
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Ginsenoside Re Improves Isoproterenol-Induced Myocardial Fibrosis and Heart Failure in Rats.Evidence-based complementary and alternative medicine : eCAM · 2019
    Article
  12. Review
  13. Cardiac Fibrosis: The Fibroblast Awakens.Circulation research · 2016
    Review
  14. Fatty old hearts: role of cardiac lipotoxicity in age-related cardiomyopathy.Pathobiology of aging & age related diseases · 2016
    Review
  15. Article
  16. Estrogen and the female heart.Molecular and cellular endocrinology · 2014
    Review
  17. Review
  18. Review
  19. Review
  20. Transient receptor potential (TRP) channels and cardiac fibrosis.Current topics in medicinal chemistry · 2013
    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

2 authors at 1 institution in 1 country.

Shogen IsoyamaTohoku Bunka Gakuen University, Faculty of Medical Science and Welfare, 6-45-16 Kunimi, Aoba-ku, Sendai 981-8551, Japan. shogen@rehab.tbgu.ac.jp
Yuko Nitta-Komatsubara
Tohoku Bunka Gakuen University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Congestive heart failure occurs more frequently in older individuals. This higher incidence of heart failure may be caused by the diminished capacity of aged hearts to adapt to increased hemodynamic overload and ischemia which are the most important triggers for heart failure in the aged. In the immediate early phase after the imposition of ascending aortic banding, the mRNA expression of proto-oncogenes (c-fos, c-jun and c-myc) was diminished in aged rat hearts compared with young adult hearts. In the later phase, the pattern of expression of contractile protein genes in aged hearts differed quantitatively from that in adult hearts. The hypertrophic responses to the imposition of not only pressure-overload but also volume-overload were also diminished at the organ and cellular levels. In addition, this diminution was observed both in the left and right ventricles. Against ischemic insults, aged hearts responded with a diminished expression of proto-oncogenes and heat shock proteins. Thus, aged hearts are characterized by poor adaptation to hemodynamic overload and by a poor self-protective mechanism against cell death through necrosis and apoptosis. Of interest, more severe hemodynamic overload elevated the diminished responses to a level similar to that in adult hearts, suggesting that the threshold for the heart to respond to hemodynamic overload or ischemia is elevated in aged hearts. In addition, even in aged hearts ischemic preconditioning upregulated the diminished gene expression in a gene-dependent manner. Thus, the capacity for adaptation to hemodynamic overload and ischemia is diminished in aged hearts, but aged hearts preserve the ability to respond to these under some conditions.

Indexed as

Adaptation, PhysiologicalAgedAgingAnimalsHeart FailureHemodynamicsHumansMyocardial IschemiaRatsVentricular Function

Identifiers

PMID11790923
OpenAlexW1608587263

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.