ArticleRenal failure2025
Inhibition of matrix metalloproteinase-9 attenuates kidney fibrosis and cellular senescence in the transition from acute kidney injury to chronic kidney disease.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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
7 citing papers in PubMed.
- Per- and polyfluoroalkyl substances and kidney disease: Genetic associations and computational prioritization of candidate toxicogenomic pathways.PLoS computational biology · 2026Article
- Degradable MMP9-responsive high-density lipoprotein nanoparticles enable efficient siRNA-PGRN and quercetin delivery to remodel the fibrotic microenvironment and attenuate renal fibrosis.Journal of nanobiotechnology · 2026Article
- Neutrophil-Driven Cascade-Targeted Nanocarriers Restore Mitochondrial Homeostasis to Ameliorate Renal Ischemia-Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting cellular senescence in diabetic kidney disease: potential of regenerative, cell-based therapies and other senotherapeutic approaches.Kidney international · 2026Review
- Proteomics of aging: biomarkers for physiological systems and diseases.Frontiers in aging · 2026Review
- Ligature-induced periodontitis in mice potentially accelerates CD4Frontiers in immunology · 2026Article
- Matrix Metalloproteinase-9 (MMP-9) as a Therapeutic Target: Insights into Molecular Pathways and Clinical Applications.Pharmaceutics · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe mechanisms underlying the progression of chronic kidney disease (CKD) following acute kidney injury (AKI) remain poorly understood. Senescent cells induce maladaptive repair have been identified as a significant contributor to CKD subsequent to AKI. PURPOSE: The purpose of this study was to investigate the correlations between kidney fibrosis after unilateral ischemia injury and cellular senescence and explored the potential therapeutic effect of GM6001 on AKI to CKD transition.
resultsThe study revealed a progressive increase in both fibrosis and matrix metalloproteinase 9 (MMP9) expression, peaking approximately 14 days following unilateral ischemic injury, indicating a pivotal role of MMP9 in the pathogenesis of renal fibrosis. Additionally, the research identified an elevation in markers of renal senescence over time, including SA-β-gal, P53, P21, and P16. Treatment with GM6001 demonstrated a significant reduction in both fibrosis and senescence, evidenced by decreased MMP9 expression and associated fibrotic markers, alongside improvements in cellular senescence indicators.
conclusionThe study provided compelling evidence on the role of MMP9 in the progression of renal fibrosis and the transition from AKI to CKD. The early activation of MMP9 and its association with fibrosis highlighted its potential as a therapeutic target. GM6001, through its inhibition of MMP9, offered a promising avenue for reducing both fibrosis and cellular senescence, suggesting its potential utility in ameliorating CKD.
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