ArticleAmerican journal of physiology. Heart and circulatory physiology2020
Pressure overload generates a cardiac-specific profile of inflammatory mediators.
Article in American journal of physiology. Heart and circulatory physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- What Explains the Pattern of Fibrosis in Chronic Graft-Versus-Host Disease?Clinical transplantation · 2026Review
- Inflammation, metabolism, and aging in heart failure with preserved ejection fraction: Mechanisms and treatment perspectives.Journal of translational internal medicine · 2026Article
- Left ventricular hypertrophy and myocardial fibrosis in heart failure with preserved ejection fraction: mechanisms and treatment.European heart journal · 2026Review
- Cellular senescence in Crohn's disease: a double-edged sword in intestinal fibrosis.Frontiers in immunology · 2026Review
- Persistent Fibrosis in Heart Failure With a Reduced Ejection Fraction Linked to Phenotypic Differences in Human Cardiac Fibroblast Populations.Journal of the American Heart Association · 2025Article
- Identification of molecular signatures in epicardial adipose tissue in heart failure with preserved ejection fraction.ESC heart failure · 2024Article
- Role of macrophages in regression of myocardial fibrosis following alleviation of left ventricular pressure overload.American journal of physiology. Heart and circulatory physiology · 2024Article
- Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure.Autophagy reports · 2024Review
- Left Ventricular Gene Expression in Heart Failure With Preserved Ejection Fraction-Profibrotic and Proinflammatory Pathways and Genes.Circulation. Heart failure · 2023Article
- Characterizing and Quenching Autofluorescence in Fixed Mouse Adrenal Cortex Tissue.International journal of molecular sciences · 2023Article
- Mechanisms that limit regression of myocardial fibrosis following removal of left ventricular pressure overload.American journal of physiology. Heart and circulatory physiology · 2022Article
- New Progress in the Molecular Regulations and Therapeutic Applications in Cardiac Oxidative Damage Caused by Pressure Overload.Antioxidants (Basel, Switzerland) · 2022Review
- Article
- Organized Chaos: Deciphering Immune Cell Heterogeneity's Role in Inflammation in the Heart.Biomolecules · 2021Review
- From Systemic Inflammation to Myocardial Fibrosis: The Heart Failure With Preserved Ejection Fraction Paradigm Revisited.Circulation research · 2021Review
- Myokines and Heart Failure: Challenging Role in Adverse Cardiac Remodeling, Myopathy, and Clinical Outcomes.Disease markers · 2021Review
- Injury-specific inflammation leads to organ-specific fibrosis.American journal of physiology. Heart and circulatory physiology · 2020Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Mechanisms that contribute to myocardial fibrosis, particularly in response to left ventricular pressure overload (LVPO), remain poorly defined. To test the hypothesis that a myocardial-specific profile of secreted factors is produced in response to PO, levels of 44 factors implicated in immune cell recruitment and function were assessed in a murine model of cardiac hypertrophy and compared with levels produced in a model of pulmonary fibrosis (PF). Mice subjected to PO were assessed at 1 and 4 wk. Protein from plasma, LV, lungs, and kidneys were analyzed by specific protein array analysis in parallel with protein from mice subjected to silica-instilled PF. Of the 44 factors assessed, 13 proteins were elevated in 1-wk PO myocardium, whereas 18 proteins were found increased in fibrotic lung. Eight of those increased in 1-wk LVPO were not found to be increased in fibrotic lungs (CCL-11, CCL-12, CCL-17, CCL-19, CCL-21, CCL-22, IL-16, and VEGF). Additionally, six factors were increased in plasma of 1-wk LVPO in the absence of increases in myocardial levels. In contrast, in mice with PF, no factors were found increased in plasma that were not elevated in lung tissue. Of those factors increased at 1 wk, only TIMP-1 remained elevated at 4 wk of LVPO. Immunohistochemistry of myocardial vasculature at 1 and 4 wk revealed similar amounts of total vasculature; however, evidence of activated endothelium was observed at 1 wk and, to a lesser extent, at 4 wk LVPO. In conclusion, PO myocardium generated a unique signature of cytokine expression versus that of fibrotic lung.
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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.