ArticleCell death & disease2017
ErbB4 signaling stimulates pro-inflammatory macrophage apoptosis and limits colonic inflammation.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
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- Neuregulin 4-dependent MAPK amplification mediates urate-induced β-cell dysfunction.Journal of diabetes investigation · 2026Article
- The adipose tissue-plaque crosstalk: omics profiling of perivascular adipose tissues for understanding plaque stability.Cardiovascular diabetology · 2026Review
- Neuregulin 4 in Insulin Resistance: Mechanisms, Controversies, and Therapeutic Perspectives.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Hirschsprung's disease may increase the incidence of inflammatory bowel disease through alterations in CA1.Pediatric research · 2025Article
- Neuregulin 4 inhibits synovial macrophage pro-inflammatory polarization via ErbB4/Stat5b/NF-κB signaling to alleviate osteoarthritis progression.Journal of orthopaedic surgery and research · 2025Article
- Targeted activation of ErbB4 receptor ameliorates neuronal deficits and neuroinflammation in a food-borne polystyrene microplastic exposed mouse model.Journal of neuroinflammation · 2025Article
- Cellular interactions within the immune microenvironment underpins resistance to cell cycle inhibition in breast cancers.Nature communications · 2025Article
- Application of Nanomaterials in Early Imaging and Advanced Treatment of Atherosclerosis.Chemical & biomedical imaging · 2025Review
- Role of Long Non-Coding RNA GUSBP11 in Chronic Periodontitis Through Regulation of miR-185-5p: A Retrospective Cohort Study.Journal of inflammation research · 2025Article
- Short-term heavy drinking in a non-human primate model skews monocytes toward a hypo-inflammatory phenotype.Frontiers in immunology · 2025Article
- Complex networks interactions between bioactive compounds and adipose tissue vis-à-vis insulin resistance.Frontiers in endocrinology · 2025Article
- Proteome-wide mendelian randomization identifies novel therapeutic targets for chronic kidney disease.Scientific reports · 2024Article
- Brown adipose tissue-derived FGF21 mediates the cardioprotection of dexmedetomidine in myocardial ischemia/reperfusion injury.Scientific reports · 2024Article
- Intestinal permeability correlates with disease activity and DNA methylation changes in lupus patients.Clinical immunology (Orlando, Fla.) · 2024Article
- Mucosal immune responses toMarine life science & technology · 2024Article
- The journey towards physiology and pathology: Tracing the path of neuregulin 4.Genes & diseases · 2024Review
- The Potential of Neuregulin 4 as a Novel Biomarker and Therapeutic Agent for Vascular Complications in Type 2 Diabetes Mellitus.Journal of inflammation research · 2024Review
- The role of novel adipokines in hepatocellular carcinoma progression: a mini review.American journal of cancer research · 2024Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Efficient clearance of pro-inflammatory macrophages from tissues after resolution of a challenge is critical to prevent prolonged inflammation. Defects in clearance can contribute to conditions such as inflammatory bowel disease, and thus may be therapeutically targetable. However, the signaling pathways that induce termination of pro-inflammatory macrophages are incompletely defined. We tested whether the ErbB4 receptor tyrosine kinase, previously not known to have role in macrophage biology, is involved in this process. In vitro, pro-inflammatory activation of cultured murine and human macrophages induced ErbB4 expression; in contrast, other ErbB family members were not induced in pro-inflammatory cells, and other innate immune lineages (dendritic cells, neutrophils) did not express detectable ErbB4 levels. Treatment of activated pro-inflammatory macrophages with the ErbB4 ligand neuregulin-4 (NRG4) induced apoptosis. ErbB4 localized to the mitochondria in these cells. Apoptosis was accompanied by loss of mitochondrial membrane potential, and was dependent upon the proteases that generate the cleaved ErbB4 intracellular domain fragment, suggesting a requirement for this fragment and mitochondrial pathway apoptosis. In vivo, ErbB4 was highly expressed on pro-inflammatory macrophages but not neutrophils during experimental DSS colitis in C57Bl/6 mice. Active inflammation in this model suppressed NRG4 expression, which may allow for macrophage persistence and ongoing inflammation. Consistent with this notion, NRG4 levels rebounded during the recovery phase, and administration of exogenous NRG4 during colitis reduced colonic macrophage numbers and ameliorated inflammation. These data define a novel role for ErbB4 in macrophage apoptosis, and outline a mechanism of feedback inhibition that may promote resolution of colitis.
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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.