ArticleJACC. Basic to translational science2023
Macrophage-Specific NLRC5 Protects From Cardiac Remodeling Through Interaction With HSPA8.
Article in JACC. Basic to translational science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
The trial behind it
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Who cites it
19 citing papers in PubMed, 21 citations in OpenAlex.
- Myocardial Fibrosis in Hypertrophic Cardiomyopathy: Leveraging Quantitative Imaging and Artificial Intelligence for Precision Management.Reviews in cardiovascular medicine · 2026Review
- Inhibition of HSPA8 alleviates experimental autoimmune encephalomyelitis via dual modulation of NLRP3 inflammasome activation: suppressing both NF-κB-mediated priming and ASC-dependent assembly.Cell death discovery · 2026Article
- Integrative Transcriptomics and Machine Learning Identify Macrophage-Associated Biomarkers in Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2026Article
- METTL3-driven mFrontiers in immunology · 2026Article
- CUGBP Elav-like family member 4 promotes cardiac remodeling through Inhibition of FMO2.BMC cardiovascular disorders · 2025Article
- Asb10 accelerates pathological cardiac remodeling by stabilizing HSP70.Cell death & disease · 2025Article
- Phenotype-Based Classification of Obstructive Hypertrophic Cardiomyopathy Undergoing Myectomy.JACC. Basic to translational science · 2025Article
- Targeting NLRC5 in cardiomyocytes protects postinfarction cardiac injury by enhancing autophagy flux through the CAVIN1/CAV1 axis.Communications biology · 2025Article
- Innate Immune Sensors and Cell Death-Frontiers Coordinating Homeostasis, Immunity, and Inflammation in Skin.Viruses · 2025Review
- Exploring Anti-Inflammatory Treatment as Upstream Therapy in the Management of Atrial Fibrillation.Journal of clinical medicine · 2025Review
- Construction of a competitive endogenous RNA network and identification of potential regulatory axes in hypertrophic cardiomyopathy.Frontiers in cardiovascular medicine · 2025Article
- Integration of multi-omics and machine learning strategies identifies immune related candidate biomarkers in inflammation-associated hypertrophic cardiomyopathy.Frontiers in immunology · 2025Article
- Pyroptosis in cardiovascular diseases: molecular mechanisms, pathological roles, and therapeutic implications.American journal of cardiovascular disease · 2025Review
- Review
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Adaptor molecules mediate negative regulation of macrophage inflammatory pathways: a closer look.Frontiers in immunology · 2024Review
- The Binding of HSPA8 and Mitochondrial ALDH2 Mediates Oxygen-Glucose Deprivation-Induced Fibroblast Senescence.Antioxidants (Basel, Switzerland) · 2023Article
- Association betweenGenes · 2023Article
- The Many Faces of NLRs in Macrophage Biology.JACC. Basic to translational science · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages regulate inflammation and the process of tissue repair. Therefore, a better understanding of macrophages in the pathogenesis of heart failure is needed. In patients with hypertrophic cardiomyopathy, NLRC5 was significantly increased in circulating monocytes and cardiac macrophages. Myeloid-specific deletion of NLRC5 aggravated pressure overload-induced pathological cardiac remodeling and inflammation. Mechanistically, NLRC5 interacted with HSPA8 and suppressed NF-κB pathway in macrophages. The absence of NLRC5 in macrophages promoted the secretion of cytokines such as interleukin-6 (IL-6), which affected cardiomyocyte hypertrophy and cardiac fibroblast activation. Tocilizumab, an anti-IL-6 receptor antagonist, may be a novel therapeutic strategy for cardiac remodeling and chronic heart failure.
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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.