ArticleKidney international2015
Lack of hyaluronidases exacerbates renal post-ischemic injury, inflammation, and fibrosis.
Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Human Recombinant Hyaluronidase Injections For Upper Limb Muscle Stiffness in Individuals With Cerebral Injury: A Case Series.EBioMedicine · 2016Trial
- Pathophysiology and Management of Sepsis-associated Acute Kidney Injury.Clinics in chest medicine · 2026Review
- Sirt6 deficiency in mast cells promotes adipose fibroinflammation in obesity through galectin-3 signaling.Nature communications · 2026Article
- Role of the endothelial cell glycocalyx in sepsis-induced acute kidney injury.Frontiers in medicine · 2025Review
- Hyaluronidase inhibitor sHA2.75 alleviates ischemia-reperfusion-induced acute kidney injury.Cell cycle (Georgetown, Tex.) · 2024Article
- HYAL1 deficiency attenuates lipopolysaccharide-triggered renal injury and endothelial glycocalyx breakdown in septic AKI in mice.Renal failure · 2023Article
- Effects of contralateral nephrectomy timing and ischemic conditions on kidney fibrosis after unilateral kidney ischemia-reperfusion injury.Renal failure · 2022Article
- Hyaluronan, a double-edged sword in kidney diseases.Pediatric nephrology (Berlin, Germany) · 2022Review
- Review
- Endogenously-Produced Hyaluronan and Its Potential to Regulate the Development of Peritoneal Adhesions.Biomolecules · 2021Review
- Macrophage-stroma interactions in fibrosis: biochemical, biophysical, and cellular perspectives.The Journal of pathology · 2021Review
- The Endothelial Glycocalyx as a Target of Ischemia and Reperfusion Injury in Kidney Transplantation-Where Have We Gone So Far?International journal of molecular sciences · 2021Review
- A two-stage bilateral ischemia-reperfusion injury-induced AKI to CKD transition model in mice.American journal of physiology. Renal physiology · 2020Article
- Hyaluronidase-2 Regulates RhoA Signaling, Myofibroblast Contractility, and Other Key Profibrotic Myofibroblast Functions.The American journal of pathology · 2020Article
- New mouse model of chronic kidney disease transitioned from ischemic acute kidney injury.American journal of physiology. Renal physiology · 2019Article
- Targeting Mechanics-Induced Fibroblast Activation through CD44-RhoA-YAP Pathway Ameliorates Crystalline Silica-Induced Silicosis.Theranostics · 2019Article
- Rodent models of AKI-CKD transition.American journal of physiology. Renal physiology · 2018Review
- Advances in Renal Cell Imaging.Seminars in nephrology · 2018Review
- Hyaluronan Production by Renomedullary Interstitial Cells: Influence of Endothelin, Angiotensin II and Vasopressin.International journal of molecular sciences · 2017Article
- Targeted HAS2 Expression Lessens Airway Responsiveness in Chronic Murine Allergic Airway Disease.American journal of respiratory cell and molecular biology · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal ischemia-reperfusion injury (IRI) is a pathological process that may lead to acute renal failure and chronic dysfunction in renal allografts. During IRI, hyaluronan (HA) accumulates in the kidney, but suppression of HA accumulation during IRI protects the kidney from ischemic insults. Here we tested whether Hyal1-/- and Hyal2-/- mice display exacerbated renal damage following unilateral IRI due to a higher HA accumulation in the post-ischemic kidney compared with that in the kidney of wild-type mice. Two days after IRI in male mice there was accumulation of HA and CD44 in the kidney, marked tubular damage, infiltration, and increase creatininemia in wild-type mice. Knockout mice exhibited higher amounts of HA and higher creatininemia. Seven days after injury, wild-type mice had a significant decrease in renal damage, but knockout mice still displayed exacerbated inflammation. HA and CD44 together with α-smooth muscle actin and collagen types I and III expression were increased in knockout compared with wild-type mice 30 days after IRI. Thus, both HA-degrading enzymes seem to be protective against IRI most likely by reducing HA accumulation in the post-ischemic kidney and decreasing the inflammatory processes. Deficiency in either HYAL1 or HYAL2 leads to enhanced HA accumulation in the post-ischemic kidney and consequently worsened inflammatory response, increased tubular damage, and fibrosis.
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