ArticleNature communications2015
CD163 interacts with TWEAK to regulate tissue regeneration after ischaemic injury.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
What it found
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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
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
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- A potential fate decision landscape of the TWEAK/Fn14 axis on stem and progenitor cells: a systematic review.Stem cell research & therapy · 2022Pooled it
- Human skeletal muscle macrophages increase following cycle training and are associated with adaptations that may facilitate growth.Scientific reports · 2019Trial
- TWEAK-induced alternative NF-κB signaling regulates Cxcl10 and Mymx to promote myoblast-to-myotube fusion and muscle regeneration.Communications biology · 2026Article
- In Vitro Analysis of TWEAK/Fn14 Axis in the Blood-Brain Barrier Models during Oxygen-Glucose Deprivation and Reoxygenation.Molecular neurobiology · 2026Article
- Research progress on TWEAK/Fn14 signaling in chronic wound healing.Frontiers in surgery · 2026Review
- Transcriptomic suppression of immune and ECM stability in skeletal muscle of patients with chronic kidney disease.PloS one · 2026Article
- Perisurgical colony stimulating factor one treatment ameliorates liver ischaemia/reperfusion injury in rats.World journal of gastroenterology · 2025Article
- Baicalin Alleviates Piglet Immunosuppression Induced byBiomolecules · 2025Article
- Review
- Unraveling the bidirectional relationship between muscle inflammation and satellite cells activity: influencing factors and insights.Journal of muscle research and cell motility · 2025Review
- CD163, a novel receptor for TNF, was revealedHeliyon · 2025Article
- TWEAK-Fn14: a promising target for cardio-cerebrovascular diseases and brain-heart syndrome.Frontiers in immunology · 2025Review
- The CD163/TWEAK/Fn14 axis: A potential therapeutic target for alleviating inflammatory bone loss.Journal of orthopaedic translation · 2024Article
- Review
- Releasable, Immune-Instructive, Bioinspired Multilayer Coating Resists Implant-Induced Fibrosis while Accelerating Tissue Repair.Advanced healthcare materials · 2024Article
- Article
- Sex-dimorphic neuroprotective effect of CD163 in an α-synuclein mouse model of Parkinson's disease.NPJ Parkinson's disease · 2023Article
- Review
- CD163+ macrophages restrain vascular calcification, promoting the development of high-risk plaque.JCI insight · 2023Article
- Baseline interleukin-10, CD163, and tumor necrosis factor-like weak inducer of apoptosis (TWEAK) gingival tissue levels in relation to clinical periodontal treatment outcomes: A 12-week follow-up study.Journal of periodontology · 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
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Macrophages are an essential component of the immune response to ischaemic injury and play an important role in promoting inflammation and its resolution, which is necessary for tissue repair. The type I transmembrane glycoprotein CD163 is exclusively expressed on macrophages, where it acts as a receptor for haemoglobin:haptoglobin complexes. An extracellular portion of CD163 circulates in the blood as a soluble protein, for which no physiological function has so far been described. Here we show that during ischaemia, soluble CD163 functions as a decoy receptor for TWEAK, a secreted pro-inflammatory cytokine of the tumour necrosis factor family, to regulate TWEAK-induced activation of canonical nuclear factor-κB (NF-κB) and Notch signalling necessary for myogenic progenitor cell proliferation. Mice with deletion of CD163 have transiently elevated levels of TWEAK, which stimulate muscle satellite cell proliferation and tissue regeneration in their ischaemic and non-ischaemic limbs. These results reveal a role for soluble CD163 in regulating muscle regeneration after ischaemic injury.
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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.