ArticleMolecular therapy : the journal of the American Society of Gene Therapy2017
Macrophage-Derived mir-155-Containing Exosomes Suppress Fibroblast Proliferation and Promote Fibroblast Inflammation during Cardiac Injury.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 276 papers, 3 of them syntheses that pooled it.
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Who cites it
276 citing papers in PubMed, 3 syntheses or guidelines pooled it, 396 citations in OpenAlex.
- Advances in the study of exosomes in cardiovascular diseases.Journal of advanced research · 2024Pooled it
- Crosstalk between fibroblasts and immunocytes in fibrosis: From molecular mechanisms to clinical trials.Clinical and translational medicine · 2024Pooled it
- Progress in research on the role of exosomal miRNAs in the diagnosis and treatment of cardiovascular diseases.Frontiers in genetics · 2022Pooled it
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Intercellular transfer of LncRNABiochemistry and biophysics reports · 2026Article
- Myocardial Ischemia-Reperfusion Injury: Molecular Mechanisms and Innovative Therapeutic Strategies.Reviews in cardiovascular medicine · 2026Review
- MicroRNAs and SGLT2 inhibitors in cardiovascular disease: Shared pathways and emerging roles.Journal of molecular and cellular cardiology plus · 2026Review
- Extracellular Vesicles in Cardiovascular Disease: Intercellular Signaling, Liquid Biopsy Biomarkers, and Therapeutic Translation.Circulation research · 2026Review
- Macrophage regulation of extracellular matrix remodeling in aging skeletal muscle.Ageing research reviews · 2026Review
- The role of non-coding RNAs derived from macrophage exosomes in cardiovascular diseases.The Journal of physiology · 2026Review
- Extracellular Vesicles in Cardiac Cell Crosstalk: from Intercellular Communication to Clinical Translation.Cardiovascular drugs and therapy · 2026Review
- Macrophage-derived exosomes in bone tissue regeneration: spatiotemporal immunomodulation, engineering advances, and translational frontiers.Journal of translational medicine · 2026Review
- Shenfu Injection Inhibits Cardiac Fibroblast Activation and Improves Myocardial Fibrosis by Down-regulating M1 Macrophage-Derived Exosomal miR-155-5p.Cardiovascular drugs and therapy · 2026Article
- Mapping the miRNA landscape of primitive macrophage extracellular vesicles highlights their pro-vasculogenic effects in engineered human cardiac tissue.APL bioengineering · 2026Article
- Engineered ATP-loaded extracellular vesicles: a dual-functional strategy for improving myocardial infarction therapy.Drug delivery and translational research · 2026Article
- Predictive Biomarkers for Coronary Collateral Circulation Development After Myocardial Infarction.International journal of molecular sciences · 2026Review
- Extracellular vesicles in the heart: mediators of intercellular communication in health and disease in vitro.Cell communication and signaling : CCS · 2026Review
- Extracellular Vesicles in the Gut-Vascular-Brain Axis: A Missing Mechanistic Link Between IBD and Stroke Risk.Biomolecules · 2026Review
- Look Who Is Talking: Extracellular Vesicles as Mediators of Intercellular and Interorgan Communication.Comprehensive Physiology · 2026Review
- Small vesicles, big potential: A review of innovative exosome delivery and molecular mechanisms in preclinical myocardial infarction models.Animal models and experimental medicine · 2026Review
216 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation plays an important role in cardiac injuries. Here, we examined the role of miRNA in regulating inflammation and cardiac injury during myocardial infarction. We showed that mir-155 expression was increased in the mouse heart after myocardial infarction. Upregulated mir-155 was primarily presented in macrophages and cardiac fibroblasts of injured hearts, while pri-mir-155 was only expressed in macrophages. mir-155 was also presented in exosomes derived from macrophages, and it can be transferred into cardiac fibroblasts by macrophage-derived exosomes. A mir-155 mimic or mir-155 containing exosomes inhibited cardiac fibroblast proliferation by downregulating Son of Sevenless 1 expression and promoted inflammation by decreasing Suppressor of Cytokine Signaling 1 expression. These effects were reversed by the addition of a mir-155 inhibitor. In vivo, mir-155-deficient mice showed a significant reduction of the incidence of cardiac rupture and an improved cardiac function compared with wild-type mice. Moreover, transfusion of wild-type macrophage exosomes to mir-155
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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.