ArticlePhysiological reports2019
Chymase inhibition retards albuminuria in type 2 diabetes.
Article in Physiological reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Crosstalk between ferroptosis and innate immune in diabetic kidney disease: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Mast Cell Chymase and Kidney Disease.International journal of molecular sciences · 2020Review
- Chymase as a Possible Therapeutic Target for Amelioration of Non-Alcoholic Steatohepatitis.International journal of molecular sciences · 2020Review
- Mechanism of Albuminuria Reduction by Chymase Inhibition in Diabetic Mice.International journal of molecular sciences · 2020Article
- Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy.International journal of molecular sciences · 2020Review
- Novel Insight into the in vivo Function of Mast Cell Chymase: Lessons from Knockouts and Inhibitors.Journal of innate immunity · 2020Review
- Chymase inhibition retards albuminuria in type 2 diabetes.Physiological reports · 2019Article
- Is chymase 1 a therapeutic target in cardiovascular disease?Expert opinion on therapeutic targetsReview
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Chymase released from mast cells produces pro-fibrotic, inflammatory, and vasoconstrictor agents. Studies were performed to test the hypothesis that chronic chymase inhibition provides a renal protective effect in type 2 diabetes. Diabetic (db/db) and control mice (db/m) were chronically infused with a chymase-specific inhibitor or vehicle for 8 weeks. Baseline urinary albumin excretion (UalbV) averaged 42 ± 3 and 442 ± 32 microg/d in control (n = 22) and diabetic mice (n = 27), respectively (p < .05). After administration of chymase inhibitor to diabetic mice, the change in UalbV was significantly lower (459 ± 57 microg/d) than in vehicle-treated diabetic mice (645 ± 108 microg/d). U
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Registered trials
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