ArticleAmerican journal of physiology. Renal physiology2011
MMP-9 gene deletion mitigates microvascular loss in a model of ischemic acute kidney injury.
Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 62 citations in OpenAlex.
- LYVE1 ectodomain shedding blunts lymphatic transmigration and clearance of macrophages during kidney injury.JCI insight · 2026Article
- Glomerular Transcriptome Analysis Reveals Endothelial Disturbances in Patients With Idiopathic Nephrotic Syndrome.Kidney medicine · 2026Article
- Elevated FTO alleviates sepsis‑induced acute kidney injury by regulating macrophage inflammatory phenotypes.International journal of molecular medicine · 2026Article
- Pharmacological Potential of Cafestol, a Bioactive Substance in Coffee, in Preventing Ischemia-Reperfusion-Induced Acute Kidney Injury.ACS omega · 2025Article
- TIMP4 as a Potential Complementary Biomarker and Therapeutic Target in Membranous Nephropathy: A Multi-Omics Investigation with Clinical Validation.Journal of inflammation research · 2025Article
- Article
- Deciphering cellular heterogeneity and pathway dynamics in urinary samples: a UMAP-Based approach to understanding acute kidney injury.Frontiers in pharmacology · 2025Article
- Matrix metalloproteinases in kidney homeostasis and diseases: an update.American journal of physiology. Renal physiology · 2024Review
- The Expression and Molecular Mechanisms of Matrix Metalloproteinase- 9 and Vascular Endothelial Growth Factor in Renal Interstitial Fibrosis in Rats.Current molecular medicine · 2024Article
- Matrix metalloproteinase-9 regulates afferent arteriolar remodeling and function in hypertension-induced kidney disease.Kidney international · 2023Article
- Network pharmacology, molecular docking, and experimental verification reveal the mechanism of San-Huang decoction in treating acute kidney injury.Frontiers in pharmacology · 2023Article
- Obeticholic Acid Reduces Kidney Matrix Metalloproteinase Activation Following Partial Hepatic Ischemia/Reperfusion Injury in Rats.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Renoprotective Effect of Vardenafil and Avanafil in Contrast-Induced Nephropathy: Emerging Evidence from an Animal Model.Journal of personalized medicine · 2022Article
- Key metalloproteinase-mediated pathways in the kidney.Nature reviews. Nephrology · 2021Review
- Protective Effects of Liposomal Curcumin on Oxidative Stress/Antioxidant Imbalance, Metalloproteinases 2 and -9, Histological Changes and Renal Function in Experimental Nephrotoxicity Induced by Gentamicin.Antioxidants (Basel, Switzerland) · 2021Article
- Effect ofPhysiological genomics · 2019Article
- Role of Renal Hypoxia in the Progression From Acute Kidney Injury to Chronic Kidney Disease.Seminars in nephrology · 2019Review
- Matrix metalloproteinase-7 protects against acute kidney injury by priming renal tubules for survival and regeneration.Kidney international · 2019Article
- Extracellular matrix roles in cardiorenal fibrosis: Potential therapeutic targets for CVD and CKD in the elderly.Pharmacology & therapeutics · 2019Review
- Effects of CoClExperimental and therapeutic medicine · 2018Article
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Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
Abstract
Microvascular rarefaction following an episode of acute kidney injury (AKI) is associated with renal hypoxia and progression toward chronic kidney disease. The mechanisms contributing to microvascular rarefaction are not well-understood, although disruption in local angioregulatory substances is thought to contribute. Matrix metalloproteinase (MMP)-9 is an endopeptidase important in modifying the extracellular matrix (ECM) and remodeling the vasculature. We examined the role of MMP-9 gene deletion on microvascular rarefaction in a rodent model of ischemic AKI. MMP-9-null mice and background control (FVB/NJ) mice were subjected to bilateral renal artery clamping for 20 min followed by reperfusion for 14, 28, or 56 days. Serum creatinine level in MMP-9-null mice 24 h after injury [1.4 (SD 0.8) mg/dl] was not significantly different from FVB/NJ mice [1.5 (SD 0.6) mg/dl]. Four weeks after ischemic injury, FVB/NJ mice demonstrated a 30-40% loss of microvascular density compared with sham-operated (SO) mice. In contrast, microvascular density was not significantly different in the MMP-9-null mice at this time following injury compared with SO mice. FVB/NJ mice had a 50% decrease in tissue vascular endothelial growth factor (VEGF) 2 wk after ischemic insult compared with SO mice. A significant difference in VEGF was not observed in MMP-9-null mice compared with SO mice. There was no significant difference in the liberation of angioinhibitory fragments from the ECM between MMP-9-null mice and FVB/NJ mice following ischemic injury. In conclusion, MMP-9 deletion stabilizes microvascular density following ischemic AKI in part by preserving tissue VEGF levels.
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