ArticleKidney international2022
Insulin-like growth factor binding protein 7 promotes acute kidney injury by alleviating poly ADP ribose polymerase 1 degradation.
Article in Kidney international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 68 citations in OpenAlex.
- Multi-organ metabolic dysregulation and cecal microbiota alterations following black carbon exposure.Journal of advanced research · 2026Article
- Renal IGFBP6 Interacts With THBS1 to Drive Renal Cellular Senescence and Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Subcutaneous transplantation of lung organoids ameliorates vascular dementia via the IGFBP7-Ago2 mediated lung-brain axis.Journal of neuroinflammation · 2026Article
- Fumarate-induced succination of A-kinase anchor protein 12 exacerbates renal inflammation and fibrosis.The Journal of clinical investigation · 2026Article
- TRIM21-mediated ubiquitination of PARP1 regulated by the PI3K/AKT-STAT5A axis suppresses small cell lung cancer.Nature communications · 2026Article
- Endothelial cell-derived IGFBP7 suppresses angiogenesis and tumor progression in colorectal cancer via the VAPA-TGF-β1 pathway.Journal of experimental & clinical cancer research : CR · 2026Article
- Minichromosome maintenance 4 plays a key role in protecting against acute kidney injury by regulating tubular epithelial cells survival and regeneration.Journal of advanced research · 2026Article
- Research advances on acute kidney injury and brain dysfunction.Frontiers in nephrology · 2026Review
- IGFBP2 and IGFBP4 interact to activate complement pathway in diabetic kidney disease.Renal failure · 2025Article
- Renal insulin-like growth factor binding-protein 7 is a critical promoter of progressive diabetic kidney disease.Nature communications · 2025Article
- Association between serum levels of insulin-like growth factor-binding proteins at admission and outcomes at 3 months after acute ischemic stroke.Annals of medicine · 2025Article
- Inhibition of PGK1 ameliorates acute kidney injury through inactivating the PKM2/ALOX12/ferroptosis pathway in a study with male mice.Nature communications · 2025Article
- Targeting PARylated RACK1/HIF-1Acta pharmaceutica Sinica. B · 2025Article
- PARylation promotes acute kidney injuryActa pharmaceutica Sinica. B · 2025Article
- Cardiac ageing: from hallmarks to therapeutic opportunities.Cardiovascular research · 2025Review
- Renal tubular epithelial IGFBP7 interacts with PKM2 to drive renal lipid accumulation and fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Article
- Integrated analysis of COVID-19 multi-omics data for eQTLs reveals genetic mechanisms underlying disease severity.bioRxiv : the preprint server for biology · 2025Article
- IGF-Binding Protein 7 and Cadmium-Induced Hepatorenal Fibrosis.Journal of the American Society of Nephrology : JASN · 2025Article
- Vitamin C Mediates IGFBP7 to Alleviate Chronic Atrophic Gastritis via the HIF-1α/VEGF Pathway.Journal of cellular and molecular medicine · 2025Article
Corrections and comments
- Commented on byUro-Science.2023
Authors and funding
27 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The novel biomarker, insulin-like growth factor binding protein 7 (IGFBP7), is used clinically to predict different types of acute kidney injury (AKI) and has drawn significant attention as a urinary biomarker. However, as a secreted protein in the circulation of patients with AKI, it is unclear whether IGFBP7 acts as a key regulator in AKI progression, and if mechanisms underlying its upregulation still need to be determined. Here we found that IGFBP7 is highly expressed in the blood and urine of patients and mice with AKI, possibly via a c-Jun-dependent mechanism, and is positively correlated with kidney dysfunction. Global knockout of IGFBP7 ameliorated kidney dysfunction, inflammatory responses, and programmed cell death in murine models of cisplatin-, kidney ischemia/reperfusion-, and lipopolysaccharide-induced AKI. IGFBP7 mainly originated from kidney tubular epithelial cells. Conditional knockout of IGFBP7 from the kidney protected against AKI. By contrast, rescue of IGFBP7 expression in IGFBP7-knockout mice restored kidney damage and inflammation. IGFBP7 function was determined in vitro using recombinant IGFBP7 protein, IGFBP7 knockdown, or overexpression. Additionally, IGFBP7 was found to bind to poly [ADP-ribose] polymerase 1 (PARP1) and inhibit its degradation by antagonizing the E3 ubiquitin ligase ring finger protein 4 (RNF4). Thus, IGFBP7 in circulation acts as a biomarker and key mediator of AKI by inhibiting RNF4/PARP1-mediated tubular injury and inflammation. Hence, over-activation of the IGFBP7/PARP1 axis represents a promising target for AKI treatment.
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