ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025
HuR inhibition reduces post-ischemic cardiac remodeling by dampening myocyte-dependent inflammatory gene expression and the innate immune response.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- HuR-dependent expression of RyR2 contributes to calcium-mediated thermogenesis in murine brown adipocytes.Scientific reports · 2026Article
- Inhibition of HuR/ELAVL-1 attenuates fibrotic progression in Mdx mice with dilated cardiomyopathy.Cellular and molecular life sciences : CMLS · 2025Article
- Article
- HuR inhibition reduces post-ischemic cardiac remodeling by dampening myocyte-dependent inflammatory gene expression and the innate immune response.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Body fluid multiomics in 3PM-guided ischemic stroke management: health risk assessment, targeted protection against health-to-disease transition, and cost-effective personalized approach are envisaged.The EPMA journal · 2024Review
- Human Antigen R, a Myofibroblast-Specific Target in Treating Cardiac Fibrosis.JACC. Basic to translational science · 2024Article
- RNA binding proteins as mediators of pathological cardiac remodeling.Frontiers in cell and developmental biology · 2024Review
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Abstract
The RNA-binding protein human antigen R (HuR) has been shown to reduce cardiac remodeling following both myocardial infarction and cardiac pressure overload, but the full extent of the HuR-dependent mechanisms within cells of the myocardium has yet to be elucidated. Wild-type mice were subjected to 30 min of cardiac ischemia (via LAD occlusion) and treated with a novel small molecule inhibitor of HuR at the time of reperfusion, followed by direct in vivo assessment of cardiac structure and function. Direct assessment of HuR-dependent mechanisms was done in vitro using neonatal rat ventricular myocytes (NRVMs) and bone marrow-derived macrophages (BMDMs). HuR activity is increased within 2 h after ischemia/reperfusion (I/R) and is necessary for early post-I/R inflammatory gene expression in the myocardium. Despite an early reduction in inflammatory gene expression, HuR inhibition has no effect on initial infarct size at 24 h post-I/R. However, pathological remodeling is reduced with preserved cardiac function at 2 weeks post-I/R upon HuR inhibition. RNA sequencing analysis of gene expression in NRVMs treated with LPS to model damage-associated molecular pattern (DAMP)-mediated activation of toll-like receptors (TLRs) demonstrates a HuR-dependent regulation of pro-inflammatory chemokine and cytokine gene expression in cardiomyocytes. Importantly, we show that conditioned media transfer from NRVMs pre-treated with HuR inhibitor loses the ability to induce inflammatory gene expression and M1-like polarization in bone marrow-derived macrophages (BMDMs) compared to NRVMs treated with LPS alone. Functionally, HuR inhibition reduces macrophage infiltration to the post-ischemic myocardium in vivo. Additionally, we show that LPS-treated NRVMs induce the migration of peripheral blood monocytes in a HuR-dependent endocrine manner. These studies demonstrate that HuR is necessary for early pro-inflammatory gene expression in cardiomyocytes following I/R injury that subsequently mediates monocyte recruitment and macrophage activation in the post-ischemic myocardium.
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