ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Dynamic molecular and histopathological changes in the extracellular matrix and inflammation in the transition to heart failure in isolated volume overload.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 73 citations in OpenAlex.
- Mechanosensor Piezo1‑mediated smooth muscular cell pyroptosis contributes to vascular calcification.International journal of molecular medicine · 2025Article
- Dysregulated fatty acid metabolism in pericardiac adipose tissue of pulmonary hypertension due to left heart disease mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Enhanced Cardiomyocyte NLRP3 Inflammasome-Mediated Pyroptosis Promotes d-Galactose-Induced Cardiac Aging.Journal of the American Heart Association · 2024Article
- Pimobendan prevents cardiac dysfunction, mitigates cardiac mitochondrial dysfunction, and preserves myocyte ultrastructure in a rat model of mitral regurgitation.BMC veterinary research · 2023Article
- Ca2+/calmodulin-dependent protein kinase II and protein kinase G oxidation contributes to impaired sarcomeric proteins in hypertrophy model.ESC heart failure · 2022Article
- Derangements and Reversibility of Energy Metabolism in Failing Hearts Resulting from Volume Overload: Transcriptomics and Metabolomics Analyses.International journal of molecular sciences · 2022Article
- Right versus left ventricular remodeling in heart failure due to chronic volume overload.Scientific reports · 2021Article
- Hemodynamic and transcriptomic studies suggest early left ventricular dysfunction in a preclinical model of severe mitral regurgitation.The Journal of thoracic and cardiovascular surgery · 2021Article
- Computational models of cardiac hypertrophy.Progress in biophysics and molecular biology · 2021Review
- Chronic cardiac structural damage, diastolic and systolic dysfunction following acute myocardial injury due to bromine exposure in rats.Archives of toxicology · 2021Article
- NLRP3 inflammasome-mediated pyroptosis contributes to the pathogenesis of non-ischemic dilated cardiomyopathy.Redox biology · 2020Article
- Cardiac remodeling secondary to chronic volume overload is attenuated by a novel MMP9/2 blocking antibody.PloS one · 2020Article
- Programmed necrosis in cardiomyocytes: mitochondria, death receptors and beyond.British journal of pharmacology · 2019Review
- Genetic deletion of calcium/calmodulin-dependent protein kinase type II delta does not mitigate adverse myocardial remodeling in volume-overloaded hearts.Scientific reports · 2019Article
- Differential Transcriptome Profile and Exercise Capacity in Cardiac Remodeling by Pressure Overload versus Volume Overload.Journal of cardiovascular imaging · 2019Article
- Bromine inhalation mimics ischemia-reperfusion cardiomyocyte injury and calpain activation in rats.American journal of physiology. Heart and circulatory physiology · 2019Article
- Chymase inhibitors for the treatment of cardiac diseases: a patent review (2010-2018).Expert opinion on therapeutic patents · 2018Review
- A Comparison of Phenomenologic Growth Laws for Myocardial Hypertrophy.Journal Of Elasticity · 2017Article
- Interleukin-6 signaling in patients with chronic heart failure treated with cardiac resynchronization therapy.Archives of medical science : AMS · 2017Article
- Desmin loss and mitochondrial damage precede left ventricular systolic failure in volume overload heart failure.American journal of physiology. Heart and circulatory physiology · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Left ventricular (LV) volume overload (VO) causes eccentric remodeling with inflammatory cell infiltration and extracellular matrix (ECM) degradation, for which there is currently no proven therapy. To uncover new pathways that connect inflammation and ECM homeostasis with cellular dysfunction, we determined the cardiac transciptome in subacute, compensated, and decompensated stages based on in vivo hemodynamics and echocardiography in the rat with aortocaval fistula (ACF). LV dilatation at 5 wk was associated with a normal LV end-diastolic dimension-to-posterior wall thickness ratio (LVEDD/PWT; compensated), whereas the early 2-wk (subacute) and late 15-wk (decompensated) ACF groups had significant increases in LVEDD/PWT. Subacute and decompensated stages had a significant upregulation of genes related to inflammation, the ECM, the cell cycle, and apoptosis. These changes were accompanied by neutrophil and macrophage infiltration, nonmyocyte apoptosis, and interstitial collagen loss. At 15 wk, there was a 40-fold increase in the matricellular protein periostin, which inhibits connections between collagen and cells, thereby potentially mediating a side-to-side slippage of cardiomyocytes and LV dilatation. The majority of downregulated genes was composed of mitochondrial enzymes whose suppression progressed from 5 to 15 wk concomitant with LV dilatation and systolic heart failure. The profound decrease in gene expression related to fatty acid, amino acid, and glucose metabolism was associated with the downregulation of peroxisome proliferator associated receptor (PPAR)-α-related and bioenergetic-related genes at 15 wk. In VO, an early phase of inflammation subsides at 5 wk but reappears at 15 wk with marked periostin production along with the suppression of genes related to PPAR-α and energy metabolism.
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