ReviewFrontiers in cardiovascular medicine2018
Cardiomyocytes and Macrophages Discourse on the Method to Govern Cardiac Repair.
Review in Frontiers in cardiovascular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Gap junctional and ephaptic coupling in cardiac electrical propagation: homocellular and heterocellular perspectives.The Journal of physiology · 2026Review
- Functional transformation of macrophage mitochondria in cardiovascular diseases.Molecular and cellular biochemistry · 2025Review
- Construction of a competitive endogenous RNA network and identification of potential regulatory axes in hypertrophic cardiomyopathy.Frontiers in cardiovascular medicine · 2025Article
- The Immune System, An Arrow into the Heart. Principles of Cardioimmunology, An Emerging Branch in Medicine.Current vascular pharmacology · 2025Review
- Review
- Regulated Cell Death Pathways in Pathological Cardiac Hypertrophy.Reviews in cardiovascular medicine · 2024Review
- Macrophage-based therapeutic approaches for cardiovascular diseases.Basic research in cardiology · 2024Review
- Lack of STAT1 co-operative DNA binding protects against adverse cardiac remodelling in acute myocardial infarction.Frontiers in cardiovascular medicine · 2023Article
- Renewal of embryonic and neonatal-derived cardiac-resident macrophages in response to environmental cues abrogated their potential to promote cardiomyocyte proliferationActa pharmaceutica Sinica. B · 2023Article
- DAMPs Released from Proinflammatory Macrophages Induce Inflammation in Cardiomyocytes via Activation of TLR4 and TNFR.International journal of molecular sciences · 2022Article
- Tumor Necrosis Factor-Oxidative medicine and cellular longevity · 2022Article
- Cardiac Macrophages and Their Effects on Arrhythmogenesis.Frontiers in physiology · 2022Review
- Emerging Roles of the Atypical Chemokine Receptor 3 (ACKR3) in Cardiovascular Diseases.Frontiers in endocrinology · 2022Review
- The NLR family pyrin domain containing 3 inflammasome in the mechanism of electroacupuncture: Current status and future perspectives.Frontiers in aging neuroscience · 2022Review
- Early activation of the cardiac CX3CL1/CX3CR1 axis delays β-adrenergic-induced heart failure.Scientific reports · 2021Article
- Protective role of ErbB3 signaling in myeloid cells during adaptation to cardiac pressure overload.Journal of molecular and cellular cardiology · 2021Article
- New Modalities of 3D Pluripotent Stem Cell-Based Assays in Cardiovascular Toxicity.Frontiers in pharmacology · 2021Review
- Single-Cell Analysis Revealed the Role of CD8Frontiers in immunology · 2021Article
- Critical roles of macrophages in pressure overload-induced cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Cardiac Immunology: A New Era for Immune Cells in the Heart.Advances in experimental medicine and biology · 2021Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In response to pathophysiological stress, the cardiac tissue undergoes profound remodeling process that incorporates the elimination of dying resident cells, compensatory hypertrophy of functional cardiomyocytes, growth and remodeling of the vascular compartment and formation of a fibrotic scar. Accumulating evidences indicate that cardiac remodeling is, at least in part, controlled by a complex crosstalk between cardiomyocytes and macrophages. The strategic location of abundant macrophages to the proximity of cardiomyocytes suggest that they could regulate the fate of cardiomyocytes in the injured heart. As such, macrophages appear as critical support cells for cardiomyocytes and play central roles in cardiac hypertrophy, fibrosis and remodeling. Notably, the cardiac tissue expands heterogeneous population of cardiac macrophages through local proliferation of resident macrophage as well as recruitment and differentiation of blood-derived monocytes. It has also been suggested that cardiac-resident macrophages display distinct functional properties from that of monocyte-derived macrophages in cardiac tissue. Furthermore, macrophages are an overflowing source of biological entities with non-canonical roles on cardiac conduction or cardiomyocyte proliferation by regulating action potential diffusion or cardiac cell cycle reentry. Alternatively, stressed cardiomyocytes can trigger the release of a broad repertoire of instructive signals that can regulate macrophage number, skew their phenotype and therefore direct their beneficial or deleterious actions. In this review, we highlight recent discoveries describing how the intricate dialogue between cardiomyocytes and macrophages can shape the deleterious or healing signaling mechanisms in the injured cardiac tissue.
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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.