ReviewNature reviews. Nephrology2021
Key metalloproteinase-mediated pathways in the kidney.
Review in Nature reviews. Nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed.
- CD177Gut · 2026Article
- Article
- Proteomics-based clustering for higher risk of venous thromboembolism in patients with nephrotic syndrome.Research and practice in thrombosis and haemostasis · 2026Article
- Kaempferol-modified mesenchymal stem cell extracellular vesicle-mimetics promote photoaging repair by suppressing ADAM10.Cell communication and signaling : CCS · 2026Article
- LYVE1 ectodomain shedding blunts lymphatic transmigration and clearance of macrophages during kidney injury.JCI insight · 2026Article
- Gene modification: Exploring the potential in treating kidney diseases.Pharmacological research · 2026Review
- Overview of the Zinc Functional Interactome Through Health Hallmarks and Medical Conditions.Nutrients · 2026Review
- Tanshinone IIA reduces tubulointerstitial fibrosis by suppressing GSDMD-mediated pyroptosis.Pharmaceutical biology · 2025Article
- Inhibition of matrix metalloproteinase-9 attenuates kidney fibrosis and cellular senescence in the transition from acute kidney injury to chronic kidney disease.Renal failure · 2025Article
- Recreational Exercise and Inflammatory Patterns in Hashimoto's Thyroiditis: Observations from a Cross-Sectional Study.Biomolecules · 2025Observational
- Mutation in the rat interleukin 34 gene impacts macrophage development, homeostasis, and inflammation.Life science alliance · 2025Article
- Insight into blood proteinase-inhibitor system and pathogenesis of renal tuberculosis induced by phylogenomically different Mycobacterium tuberculosis strains in rabbit model.BMC nephrology · 2025Article
- ADAM10-mediated β-klotho degradation: a key to FGF21 resistance in senescent vascular endothelial cells.GeroScience · 2025Article
- Matrix metalloproteinase-10 promotes kidney fibrosis by transactivating β-catenin signaling.Cell death discovery · 2025Article
- Discovery and Characterisation of Novel Poly-Histidine-Poly-Glycine Peptides as Matrix Metalloproteinase Inhibitors.Biomolecules · 2025Article
- Article
- Article
- The multifaceted role of macrophages in kidney physiology and diseases.Frontiers in immunology · 2025Review
- Article
- MARVELD1 Promotes the Invasiveness in Pancreatic Adenocarcinoma through the Activation of Epithelial-to-Mesenchymal Transition.Protein and peptide letters · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinases (ADAMs) belong to the metzincin family of zinc-containing multidomain molecules, and can act as soluble or membrane-bound proteases. These enzymes inactivate or activate other soluble or membrane-expressed mediator molecules, which enables them to control developmental processes, tissue remodelling, inflammatory responses and proliferative signalling pathways. The dysregulation of MMPs and ADAMs has long been recognized in acute kidney injury and in chronic kidney disease, and genetic targeting of selected MMPs and ADAMs in different mouse models of kidney disease showed that they can have detrimental and protective roles. In particular, MMP-2, MMP-7, MMP-9, ADAM10 and ADAM17 have been shown to have a mainly profibrotic effect and might therefore represent therapeutic targets. Each of these proteases has been associated with a different profibrotic pathway that involves tissue remodelling, Wnt-β-catenin signalling, stem cell factor-c-kit signalling, IL-6 trans-signalling or epidermal growth factor receptor (EGFR) signalling. Broad-spectrum metalloproteinase inhibitors have been used to treat fibrotic kidney diseases experimentally but more targeted approaches have since been developed, including inhibitory antibodies, to avoid the toxic side effects initially observed with broad-spectrum inhibitors. These advances not only provide a solid foundation for additional preclinical studies but also encourage further translation into clinical research.
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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.