Evidence map›Paper›PMID 26883434›Full record

ReviewHeart failure reviews2016

The fibrosis-cell death axis in heart failure.

A Piek, R A de Boer, H H W Silljé

Open access · hybridAbstract readReview
In one paragraph

Review in Heart failure reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed
18.8field-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

161 citing papers in PubMed, 295 citations in OpenAlex.

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101 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 2 institutions in 1 country.

A PiekDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9713GZ, Groningen, The Netherlands.
R A de BoerDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9713GZ, Groningen, The Netherlands.
H H W SilljéDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9713GZ, Groningen, The Netherlands. h.h.w.sillje@umcg.nl.
University of Groningen · NLUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac stress can induce morphological, structural and functional changes of the heart, referred to as cardiac remodeling. Myocardial infarction or sustained overload as a result of pathological causes such as hypertension or valve insufficiency may result in progressive remodeling and finally lead to heart failure (HF). Whereas pathological and physiological (exercise, pregnancy) overload both stimulate cardiomyocyte growth (hypertrophy), only pathological remodeling is characterized by increased deposition of extracellular matrix proteins, termed fibrosis, and loss of cardiomyocytes by necrosis, apoptosis and/or phagocytosis. HF is strongly associated with age, and cardiomyocyte loss and fibrosis are typical signs of the aging heart. Fibrosis results in stiffening of the heart, conductivity problems and reduced oxygen diffusion, and is associated with diminished ventricular function and arrhythmias. As a consequence, the workload of cardiomyocytes in the fibrotic heart is further augmented, whereas the physiological environment is becoming less favorable. This causes additional cardiomyocyte death and replacement of lost cardiomyocytes by fibrotic material, generating a vicious cycle of further decline of cardiac function. Breaking this fibrosis-cell death axis could halt further pathological and age-related cardiac regression and potentially reverse remodeling. In this review, we will describe the interaction between cardiac fibrosis, cardiomyocyte hypertrophy and cell death, and discuss potential strategies for tackling progressive cardiac remodeling and HF.

Indexed as

Cell DeathVentricular RemodelingAnimalsArrhythmias, CardiacFibrosisHeart FailureHumansMiceMyocardial InfarctionMyocardiumMyocytes, CardiacCardiomyocyteCell deathFibroblastFibrosisHeart failureHypertrophyMyofibroblastTGFβ

Identifiers

PMID26883434
PMCPMC4762920
OpenAlexW2280484610

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.