ReviewHeart failure reviews2011
Cellular and molecular pathways to myocardial necrosis and replacement fibrosis.
Review in Heart failure reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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.
Who cites it
16 citing papers in PubMed, 56 citations in OpenAlex.
- Heart-brain axis, gliotransmitters and peripheral neurogenesis: Emerging regenerative roles of cardiac nexus glia in health and disease.World journal of cardiology · 2025Review
- Mercury-Mediated Cardiovascular Toxicity: Mechanisms and Remedies.Cardiovascular toxicology · 2025Review
- Metformin Attenuates Postinfarction Myocardial Fibrosis and Inflammation in Mice.International journal of molecular sciences · 2021Article
- Molecular Imaging Using Cardiac PET/CT: Opportunities to Harmonize Diagnosis and Therapy.Current cardiology reports · 2021Review
- The prognostic role of high-sensitivity cardiac troponin T over time in ischemic and non-ischemic heart failure.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2021Article
- Clinical Implications of Uric Acid in Heart Failure: A Comprehensive Review.Life (Basel, Switzerland) · 2021Review
- Imaging tools for assessment of myocardial fibrosis in humans: the need for greater detail.Biophysical reviews · 2020Review
- Cardiospecific deletion of αE-catenin leads to heart failure and lethality in mice.Pflugers Archiv : European journal of physiology · 2018Article
- Adult murine cardiomyocytes exhibit regenerative activity with cell cycle reentry through STAT3 in the healing process of myocarditis.Scientific reports · 2017Article
- Mst1 inhibition rescues β1-adrenergic cardiomyopathy by reducing myocyte necrosis and non-myocyte apoptosis rather than myocyte apoptosis.Basic research in cardiology · 2015Article
- Metformin attenuates myocardial remodeling and neutrophil recruitment after myocardial infarction in rat.BioImpacts : BI · 2015Article
- Proteome analysis of subsarcolemmal cardiomyocyte mitochondria: a comparison of different analytical platforms.International journal of molecular sciences · 2014Article
- Fibrosis and heart failure.Heart failure reviews · 2014Review
- Article
- Differences in left ventricular cardiomyocyte loss induced by chronic intermittent hypoxia between spontaneously hypertensive and Wistar-Kyoto rats.Sleep & breathing = Schlaf & Atmung · 2011Article
- Roles of SIRT3 in heart failure: from bench to bedside.Journal of Zhejiang University. Science. BReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Fibrosis is a fundamental component of the adverse structural remodeling of myocardium present in the failing heart. Replacement fibrosis appears at sites of previous cardiomyocyte necrosis to preserve the structural integrity of the myocardium, but not without adverse functional consequences. The extensive nature of this microscopic scarring suggests cardiomyocyte necrosis is widespread and the loss of these contractile elements, combined with fibrous tissue deposition in the form of a stiff in-series and in-parallel elastic elements, contributes to the progressive failure of this normally efficient muscular pump. Cellular and molecular studies into the signal-transducer-effector pathway involved in cardiomyocyte necrosis have identified the crucial pathogenic role of intracellular Ca2+ overloading and subsequent induction of oxidative stress, predominantly confined within its mitochondria, to be followed by the opening of the mitochondrial permeability transition pore that leads to the destruction of these organelles and cells. It is now further recognized that Ca2+ overloading of cardiac myocytes and mitochondria serves as a prooxidant and which is counterbalanced by an intrinsically coupled Zn2+ entry serving as antioxidant. The prospect of raising antioxidant defenses by increasing intracellular Zn2+ with adjuvant nutriceuticals can, therefore, be preferentially exploited to uncouple this intrinsically coupled Ca2+ - Zn2+ dyshomeostasis. Hence, novel yet simple cardioprotective strategies may be at hand that deserve to be further explored.
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What OpenQuestion holds
Registered trials
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.