Evidence map›Paper›PMID 21493924›Full record

ReviewCirculation research2011

Programmed necrosis, not apoptosis, in the heart.

Gloria Kung, Klitos Konstantinidis, Richard N Kitsis

Open access · greenAbstract readComparative StudyReview
In one paragraph

Review in Circulation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed
12.0field-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

140 citing papers in PubMed, 283 citations in OpenAlex.

  1. Article
  2. Article
  3. PPP1R3G-RIPK1-ZBP1 axis activates early-stage apoptosis and late-stage necroptosis to promote doxorubicin-induced cardiotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Cardiac redox imbalance upon disruption of selenocysteine decomposition in mice.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  5. Review
  6. Article
  7. Egg Overactivation-An Overlooked Phenomenon of Gamete Physiology.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Cardiac preservation usingFrontiers in cardiovascular medicine · 2025
    Article
  10. Review
  11. mCellular & molecular biology letters · 2024
    Article
  12. Article
  13. Article
  14. Spontaneous Overactivation ofInternational journal of molecular sciences · 2024
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

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

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

3 authors at 1 institution in 1 country.

Gloria KungWilf Family Cardiovascular Research Institute, Departments of Medicine and Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Klitos Konstantinidis
Richard N Kitsis
Albert Einstein College of Medicine · US

Funding

Training in Aging ResearchT32AG023475 · NIA · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI NIR J BARZILAI, DEREK Major HUFFMAN · 2004 to 2026
$8.6M
CARDIAC MYOCYTE APOPTOSIS--MECHANISM AND SIGNIFICANCER01HL060665 · NHLBI · YESHIVA UNIVERSITY · PI KITSIS, RICHARD N · 1998 to 2013
$5.3M
High-Throughput Screen for Small Molecules that Modulate Myocardial DamageR03DA031671 · NIDA · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI KITSIS, RICHARD N · 2011 to 2012
$83k
NHLBI NIH HHS 5R01HL060665NHLBI NIH HHS R01 HL060665NIA NIH HHS 5T32AG023475NIA NIH HHS T32 AG023475NIDA NIH HHS 1R03DA031671NIDA NIH HHS R03 DA031671
6 · The paper itself

Abstract

It is well known that apoptosis is an actively mediated cell suicide process. In contrast, necrosis, a morphologically distinct form of cell death, has traditionally been regarded as passive and unregulated. Over the past decade, however, experiments in Caenorhabditis elegans and mammalian cells have revealed that a significant proportion of necrotic death is, in fact, actively mediated by the doomed cell. Although a comprehensive understanding of necrosis is still lacking, some key molecular events have come into focus. Cardiac myocyte apoptosis and necrosis are prominent features of the major cardiac syndromes. Accordingly, the recognition of necrosis as a regulated process mandates a reexamination of cell death in the heart. This review discusses pathways that mediate programmed necrosis, how they intersect with apoptotic pathways, roles of necrosis in heart disease, and new therapeutic opportunities that the regulated nature of necrosis presents.

Indexed as

AnimalsApoptosisCell DeathHeartHumansMyocytes, CardiacNecrosis

Identifiers

PMID21493924
PMCPMC12947135
OpenAlexW2118053403

What OpenQuestion holds

Textmetadata
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.