Evidence map›Paper›PMID 24278863›Full record

ReviewJournal of exercise rehabilitation2013

Effects of aging and exercise training on apoptosis in the heart.

Hyo-Bum Kwak

Erratum issuedOpen access · diamondAbstract readReview
In one paragraph

Review in Journal of exercise rehabilitation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 98 citations in OpenAlex.

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  20. Cardiac adaptation to exercise training in health and disease.Pflugers Archiv : European journal of physiology · 2020
    Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Hyo-Bum KwakDepartment of Kinesiology, Inha University, Incheon, Korea.
Inha University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is characterized by a progressive decline in cardiac function. A critical contributor to the age-related impairment in cardiac function is the loss of cardiac myocytes through "apoptosis", or programmed cell death. Structural remodeling in the heart with advancing age includes (a) loss of cardiomyocytes, (b) reactive hypertrophy of the remaining cardiomyocytes, and (c) increased connective tissue and altered geometry. The loss of cardiomyocytes with aging occurs through apoptosis. Particularly, mitochondrial-mediated apoptotic pathway is the best characterized and believed critical in regulating apoptosis with aging, suggesting that mitochondria are very important sites of programmed cell death. It has been also reported that mitochondrial dysfunction, oxidative stress, and impaired stress response contribute to age-induced mechanical remodeling as well as apoptosis. In contrast, exercise training not only improves cardiac function, but also reduces the risk of heart disease. We recently found that aging increased mitochondrial-mediated apoptotic signaling and apoptosis in the left ventricle, while chronic exercise training was effective in diminishing mitochondrial-mediated apoptotic signaling pathways in the aging heart, as indicated by lower DNA fragmentation, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive staining, and caspase-3 cleavage, when compared with left ventricles from the age-matched sedentary group. In this review, we will provide a comprehensive update regarding the effects of aging and exercise training on apoptosis in the heart.

Indexed as

AgingApoptosisHeartMitochondriaMyocytes

Identifiers

PMID24278863
PMCPMC3836520
OpenAlexW1989446499

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.