ArticleJournal of molecular and cellular cardiology2025
Hyaluronan provokes inflammation but suppresses phagocytotic function in macrophages.
Article in Journal of molecular and cellular cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- TAK1 drives inflammatory fibroblast acquisition and shapes myocardial infarction responses in male mice.Nature communications · 2026Article
- Macrophage Efferocytosis in Heart.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Hyaluronan in cardiac disease: implications for the extracellular matrix beyond collagen.American journal of physiology. Heart and circulatory physiology · 2026Review
- Targeting efferocytosis for tissue regeneration: From microenvironment reprogramming to clinical translation.Theranostics · 2026Review
- Efferocytosis in myocardial infarction: the regulatory core from inflammation resolution to cardiac repair.Frontiers in immunology · 2026Review
- Fibroblast Has2 limits acute heart failure following myocardial infarction in male mice.Physiological reports · 2025Article
- Exercise sensitizes the pressure diuresis response: shifting immune landscapes may underlie renal adaptations.American journal of physiology. Renal physiology · 2025Article
- Pyruvate kinase splice variants in fibroblasts influence cardiac remodeling after myocardial infarction in male mice.Journal of molecular and cellular cardiology · 2025Article
- Hyaluronic Acid in Immune Response.Biomolecules · 2025Review
- Macrophage polarization in acute myocardial infarction: multidimensional regulation and emerging therapeutic opportunities.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
backgroundThe extracellular matrix (ECM) provides structural and functional support for the myocardium, but myocardial infarction (MI) changes the composition of the ECM. One of the chief components of the ECM, hyaluronan (HA), accumulates after MI; however, specific biological actions of HA-particularly at the level of infiltrating immune cells and implications of such interactions on ventricular remodeling-have not been explored. GOAL: Because acute accumulation of HA coincides with macrophage infiltration after MI, we assessed the impact of HA on macrophage function.
resultsCompared to SHAM hearts, HA levels were elevated in both the infarct and remote regions of infarcted hearts. Because acute accumulation of HA coincides with macrophage infiltration after MI, we explored the implication of HA accumulation on various endpoints of macrophage function, including macrophage activation, phagocytosis, and efferocytosis. Our data suggests that exposing macrophages to HA
conclusionHA accumulates post-MI and may promote a pro-inflammatory phenotype in macrophages. Future studies will explore the extent to which post infarct HA accumulation regulates cardiac macrophage dynamics and function in vivo.
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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.