ArticleJournal of molecular and cellular cardiology2009
Pleiotropic effects of neutrophils on myocyte apoptosis and left ventricular remodeling during early volume overload.
Article in Journal of molecular and cellular cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Contributions of mechanical loading and hormonal changes to eccentric hypertrophy during volume overload: A Bayesian analysis using logic-based network models.PLoS computational biology · 2025Article
- Left ventricular remodeling in atrial fibrillation is associated with elevated NAP-2 and 3-nitrotyrosine.Biomarkers in medicine · 2025Article
- Transcriptional meta-analysis and immune cell profiles reveal altered neutrophil dynamics in chronic atrial fibrillation.Royal Society open science · 2025Article
- Circulating neutrophil-related proteins associate with incident heart failure and cardiac dysfunction: The ARIC study.European journal of heart failure · 2023Article
- Innate Immune Cells in Pressure Overload-Induced Cardiac Hypertrophy and Remodeling.Frontiers in cell and developmental biology · 2021Review
- Effects of exogenous neurotrophin-3 on myocyte apoptosis and Ca(2+)-ATP enzyme levels following nerve injury in rats.International journal of clinical and experimental medicine · 2015Article
- Role of interleukin-6 in regulation of immune responses to remodeling after myocardial infarction.Heart failure reviews · 2015Review
- The multiple mechanistic faces of a pure volume overload: implications for therapy.The American journal of the medical sciences · 2014Review
- Acute aortocaval fistula: role of low perfusion pressure and subendocardial remodeling on left ventricular function.International journal of experimental pathology · 2013Article
- The role of type 1 angiotensin receptors on T lymphocytes in cardiovascular and renal diseases.Current hypertension reports · 2013Article
- A nonthoracotomy myocardial infarction model in an ovine using autologous platelets.BioMed research international · 2013Article
- Beta1-adrenergic receptors promote focal adhesion signaling downregulation and myocyte apoptosis in acute volume overload.Journal of molecular and cellular cardiology · 2012Article
- Dynamic molecular and histopathological changes in the extracellular matrix and inflammation in the transition to heart failure in isolated volume overload.American journal of physiology. Heart and circulatory physiology · 2011Article
- Tumor necrosis factor-alpha produced in cardiomyocytes mediates a predominant myocardial inflammatory response to stretch in early volume overload.Journal of molecular and cellular cardiology · 2010Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Most of the available evidence on the role of neutrophils on pathological cardiac remodeling has been pertained after acute myocardial infarction. However, whether neutrophils directly contribute to the pathogenesis of cardiac remodeling after events other than acute myocardial infarction remains unknown. Here we show that acute eccentric hypertrophy induced by aorto-caval fistula (ACF) in the rats induced an increase in the inflammatory response characterized by activation of the STAT pathway and increased infiltration of neutrophils in the myocardium. This early inflammation was associated with a decrease in interstitial collagen accumulation and an increase in myocyte apoptosis. Neutrophil infiltration blockade attenuated MMP activation, ECM degradation, and myocyte apoptosis induced by ACF at 24 hours and attenuated the development of eccentric hypertrophy induced by ACF at 2 and 3 weeks, suggesting a causal relationship between neutrophils and the ACF-induced cardiac remodeling. In contrast, sustained neutrophil depletion over 4 weeks resulted in adverse cardiac remodeling with further increase in cardiac dilatation and macrophage infiltration, but with no change in myocyte apoptosis level. These data support a functional role for neutrophils in MMP activation, ECM degradation, and myocyte apoptosis during eccentric cardiac hypertrophy and underscore the adverse effects of chronic anti-neutrophil therapy on cardiac remodeling induced by early volume overload.
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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.