ArticleJournal of the American Society of Nephrology : JASN2014
Thrombospondin-1 activation of signal-regulatory protein-α stimulates reactive oxygen species production and promotes renal ischemia reperfusion injury.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 61 papers, 1 of them a synthesis that pooled it.
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Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- Oxidative Stress and Cardiovascular Aging: Interaction Between NRF-2 and ADMA.Current cardiology reviews · 2017Pooled it
- ITCH-Mediated Ubiquitination and Degradation of THBS1: A Key Mechanism for Enhancing Mitochondrial Biogenesis and Alleviating Mouse Skeletal Muscle Atrophy.Acta physiologica (Oxford, England) · 2026Article
- A Biomimetic Nanoparticle System Intercepts and Degrades Thrombospondin-1 to Restore Vascular Homeostasis After Ischemic Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Thrombospondin 1 aggravates cardiac remodeling in heart failure with preserved ejection fraction by inhibiting mitophagy.iScience · 2026Article
- Endothelial IRE1α promotes thrombospondin-1 mRNA decay and supports metabolic stress adaptation of pancreatic islets.Nature communications · 2026Article
- Review
- Establishing and Validating a Biomolecular Signature of Ischemia/Reperfusion Injury in a Porcine Pancreas Allotransplantation Model.Transplantation direct · 2025Article
- CD47-mediated tumor microenvironment remodeling: a central mechanism in immune evasion.Acta biochimica et biophysica Sinica · 2025Review
- Macrophages in prostate cancer: dual roles in tumor progression and immune evasion.Journal of translational medicine · 2025Review
- Gasdermin D mutation protects against renal ischemia reperfusion injury.Physiological reports · 2025Article
- ADAMTS13 attenuates renal fibrosis by suppressing thrombospondin 1 mediated TGF-β1/Smad3 activation.Toxicology and applied pharmacology · 2025Article
- Beyond cancer: The potential application of CD47-based therapy in non-cancer diseases.Acta pharmaceutica Sinica. B · 2025Review
- Article
- Genomic Insights into Pig Domestication and Adaptation: An Integrated Approach Using Genome-Wide Selection Analysis and Multiple Public Datasets.Animals : an open access journal from MDPI · 2024Article
- Single-Cell Spatial Transcriptomics Unveils Platelet-Fueled Cycling Macrophages for Kidney Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Thrombospondin-1 Drives Cardiac Remodeling in Chronic Kidney Disease.JACC. Basic to translational science · 2024Article
- Cell-cell communication in kidney fibrosis.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024Review
- Proteomic analysis of mitochondria associated membranes in renal ischemic reperfusion injury.Journal of translational medicine · 2024Article
- Tolerating CD47.Clinical and translational medicine · 2024Review
- Nrf2 Pathway and Oxidative Stress as a Common Target for Treatment of Diabetes and Its Comorbidities.International journal of molecular sciences · 2024Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Ischemia reperfusion injury (IRI) causes tissue and organ injury, in part, through alterations in tissue blood flow and the production of reactive oxygen species. The cell surface receptor signal-regulatory protein-α (SIRP-α) is expressed on inflammatory cells and suppresses phagocytosis, but the function of SIRP-α in IRI has not been determined. We reported previously that the matricellular protein thrombospondin-1 is upregulated in IRI. Here, we report a novel interaction between thrombospondin-1 and SIRP-α on nonphagocytic cells. In cell-free experiments, thrombospondin-1 bound SIRP-α. In vascular smooth muscle cells and renal tubular epithelial cells, treatment with thrombospondin-1 led to phosphorylation of SIRP-α and downstream activation of Src homology domain 2-containing phosphatase-1. Thrombospondin-1 also stimulated phosphorylation of p47(phox) (an organizer subunit for nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 1/2) and increased production of superoxide, both of which were abrogated by knockdown or antibody blockade of SIRP-α. In rodent aortic rings, treatment with thrombospondin-1 increased the production of superoxide and inhibited nitric oxide-mediated vasodilation in a SIRP-α-dependent manner. Renal IRI upregulated the thrombospondin-1-SIRP-α signaling axis and was associated with increased superoxide production and cell death. A SIRP-α antibody that blocks thrombospondin-1 activation of SIRP-α mitigated the effects of renal IRI, increasing blood flow, suppressing production of reactive oxygen species, and preserving cellular architecture. A role for CD47 in SIRP-α activation in these pathways is also described. Overall, these results suggest that thrombospondin-1 binding to SIRP-α on nonphagocytic cells activates NADPH oxidase, limits vasodilation, and promotes renal IRI.
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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.