Evidence map›Paper›PMID 29737434›Full record

ReviewHeart failure reviews2018

Anti-apoptosis in nonmyocytes and pro-autophagy in cardiomyocytes: two strategies against postinfarction heart failure through regulation of cell death/degeneration.

Genzou Takemura, Hiromitsu Kanamori, Hideshi Okada, Nagisa Miyazaki, Takatomo Watanabe, Akiko Tsujimoto, Kazuko Goto, Rumi Maruyama, Takako Fujiwara, Hisayoshi Fujiwara

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
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  6. Article
  7. Review
  8. Article
  9. Synergistic combinations ofFrontiers in pharmacology · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Involvement of circRNAs in the Development of Heart Failure.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. MiR-199 Aggravates Doxorubicin-Induced Cardiotoxicity by Targeting TAF9b.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  20. 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

10 authors at 5 institutions in 1 country.

Genzou TakemuraDepartment of Internal Medicine, Asahi University School of Dentistry, 1851 Hozumi, Mizuho, 501-0296, Japan. gt@dent.asahi-u.ac.jp.
Hiromitsu KanamoriDepartment of Cardiology, Gifu University School of Medicine, Gifu, Japan.
Hideshi OkadaDepartment of Internal Medicine, Asahi University School of Dentistry, 1851 Hozumi, Mizuho, 501-0296, Japan.
Nagisa MiyazakiDepartment of Internal Medicine, Asahi University School of Dentistry, 1851 Hozumi, Mizuho, 501-0296, Japan.
Takatomo WatanabeDepartment of Cardiology, Gifu University School of Medicine, Gifu, Japan.
Akiko TsujimotoDepartment of Internal Medicine, Asahi University School of Dentistry, 1851 Hozumi, Mizuho, 501-0296, Japan.
Kazuko GotoDepartment of Cardiology, Gifu University School of Medicine, Gifu, Japan.
Rumi MaruyamaDepartment of Cardiology, Gifu University School of Medicine, Gifu, Japan.
Takako FujiwaraDepartment of Food and Nutrition, Sonoda Women's University, Amagasaki, Japan.
Hisayoshi FujiwaraHyogo Prefectural Amagasaki General Medical Center, Amagasaki, Japan.
Gifu University · JPAsahi University · JPMizuho (Japan) · JPHyogo Prefectural Amagasaki General Medical Center · JPSonoda Women's University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-apoptotic therapy for cardiomyocytes could be an effective strategy for preventing or treating heart failure. Notably, however, morphological evidence definitively demonstrating cardiomyocyte apoptosis has been very rare in actual heart diseases such as acute myocardial infarction and heart failure. By contrast, within the postinfarction heart, interstitial noncardiomyocytes such as granulation tissue cells do die via apoptosis to form scar tissue. Blockade of this apoptosis improves survival and mitigates ventricular remodeling and dysfunction during the chronic stage. Possible mechanisms to explain this benefit might be preservation of infarcted wall thickness and preservation of myofibroblasts, which could promote infarct shrinkage; both would reduce wall stress through Laplace's law. On the other hand, autophagy is an intracellular degradation mechanism that compensates for energy insufficiency by digesting and recycling intracellular components, and is often observed in cardiomyocytes within failing hearts with various origins including postinfarction. Starvation strongly induces and activates autophagic degeneration within cardiomyocytes. When that activation is inhibited, the starved animals suffer from heart failure. Promoting autophagy through caloric restriction or several reagents not only reduces the acute infarct size but also mitigates postinfarction cardiac remodeling and dysfunction during chronic stages. Moreover, augmenting autophagy by the treatment with resveratrol or exercise can bring about reverse remodeling in failing hearts with a large old myocardial infarction. In conclusion, we propose two strategies for managing postinfarction heart failure through control of cell death/degeneration: (1) anti-apoptosis in granulation tissue noncardiomyocytes; and (2) pro-autophagy in salvaged cardiomyocytes.

Indexed as

AnimalsApoptosisAutophagyDisease ProgressionHeart FailureHumansMyocardial InfarctionMyocardiumMyocytes, CardiacApoptosisAutophagyHeart failureRemodelingUltrastructure

Identifiers

PMID29737434
OpenAlexW2801595185

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.