Evidence map›Paper›PMID 20833960›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2010

Delayed activation of caspase-independent apoptosis during heart failure in transgenic mice overexpressing caspase inhibitor CrmA.

Soochan Bae, Parco M Siu, Sangita Choudhury, Qingen Ke, Jun H Choi, Young Y Koh, Peter M Kang

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. The Effect ofEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
  6. The Prominin-1-Derived Peptide Improves Cardiac Function Following Ischemia.International journal of molecular sciences · 2021
    Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Hydrogen peroxide-responsive copolyoxalate nanoparticles for detection and therapy of ischemia-reperfusion injury.Journal of controlled release : official journal of the Controlled Release Society · 2013
    Article
  15. Article
  16. Downregulation of doxorubicin-induced myocardial apoptosis accompanies postnatal heart maturation.American journal of physiology. Heart and circulatory physiology · 2012
    Article
  17. Review
  18. Apoptosis in Anthracycline Cardiomyopathy.Current pediatric reviews · 2011
    Article
  19. Article
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

7 authors at 1 institution in 1 country.

Soochan BaeCardiovascular Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.
Parco M Siu
Sangita Choudhury
Qingen Ke
Jun H Choi
Young Y Koh
Peter M Kang
Beth Israel Deaconess Medical Center · US

Funding

Apoptosis inducing factor in cardiac apoptosisR01HL091998 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KANG, PETER M · 2009 to 2010
$1.1M
NHLBI NIH HHS R01-HL-091998
6 · The paper itself

Abstract

Although caspase activation is generally thought to be necessary to induce apoptosis, recent evidence suggests that apoptosis can be activated in the setting of caspase inhibition. In this study, we tested the hypothesis that caspase-independent apoptotic pathways contribute to the development of heart failure in the absence of caspase activation. Acute cardiomyopathy was induced using a single dose of doxorubicin (Dox, 20 mg/kg) injected into male wild-type (WT) and transgenic (Tg) mice with a cardiac-specific expression of cytokine response modifier A (CrmA), a known caspase inhibitor. Early (6 day) survival was significantly better in CrmA Tg (81%) than WT (38%) mice. Twelve days after Dox injection, however, the mortality benefit had dissipated, and increased cardiac apoptosis was observed in both groups. There was, however, a significantly greater release of apoptosis-inducing factor (AIF) from mitochondria to cytosol in CrmA Tg compared with WT mice, which suggests that an enhancement of activation in caspase-independent apoptotic pathways had occurred. The administration of a poly(ADP-ribose) polymerase-1 inhibitor, 4-amino-1,8-naphthalimide (4-AN), to Dox-treated mice resulted in significantly improved cardiac function, a significant blockade of AIF released from mitochondria, and decreased cardiac apoptosis. There were also significantly improved survival in WT (18% without 4-AN vs. 89% with 4-AN) and CrmA Tg (13% without 4-AN vs. 93% with 4-AN) mice 12 days after Dox injection. In conclusion, these findings suggest that apoptosis can be induced in the heart lacking caspase activation via caspase-independent pathways and that enabling the inhibition of AIF activation may provide a significant cardiac benefit.

Indexed as

1-NaphthylamineAnimalsApoptosisApoptosis Inducing FactorCaspase InhibitorsCaspasesDisease Models, AnimalDoxorubicinHeart FailureMaleMiceMice, TransgenicMitochondria, HeartNaphthalimidesPoly(ADP-ribose) Polymerase InhibitorsQuinolones1-Naphthylamine4-amino-1,8-naphthalimideApoptosis Inducing FactorCaspase InhibitorsCaspasesDoxorubicininterleukin-1beta-converting enzyme inhibitorNaphthalimidesPoly(ADP-ribose) Polymerase InhibitorsQuinolonesSerpinsViral Proteins

Identifiers

PMID20833960
PMCPMC2993210
OpenAlexW2102005709

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.