Kidney or renal fibrosis is a progressive condition characterized by excessive extracellular matrix deposition, leading to renal dysfunction, and contributing to the progression of chronic kidney disease (CKD). Aragen offers several rodent models that help investigate the mechanisms of kidney fibrosis and evaluate potential therapies. These models include:
- Unilateral Ureteral Obstruction (UUO): A widely used model for studying renal fibrosis.
- Sodium Oxalate-Induced: Used to study kidney injury and fibrosis due to crystal formation.
- Adenine-Induced: Models the progression of CKD.
- 5/6 Nephrectomy: Simulates progressive renal dysfunction and fibrosis.
These models are essential for understanding kidney fibrosis in CKD and testing novel anti-fibrotic treatments.
Unilateral Ureteral Obstruction (UUO) Mice Model
The Unilateral Ureteral Obstruction (UUO) model is widely used to induce kidney fibrosis in mice model, mimicking chronic obstructive nephropathy in humans. It causes tubular injury and fibrosis in the obstructed kidney, making it a key tool for studying chronic kidney disease (CKD), renal inflammation, and tissue remodelling. The UUO animal model is commonly used to evaluate therapies targeting renal fibrosis and CKD progression.
Aragen offers preclinical UUO models and tailored services to support research and accelerate the development of anti-fibrotic treatments.
Sodium Oxalate-Induced Animal Model
Sodium oxalate is a compound that can induce crystal formation in the kidneys, leading to both kidney injury and fibrosis, often seen in conditions like nephrolithiasis and hyperoxaluria. This model helps researchers to study the molecular mechanisms of crystal-induced kidney injury, inflammation, and fibrosis. It also provides a platform for testing potential treatments aimed at preventing or reversing kidney damage caused by oxalate crystals.
Adenine-Induced Animal Model
Adenine-induced kidney fibrosis model is used to mimic the progression of CKD by inducing tubulointerstitial fibrosis through the administration of adenine, which results in renal impairment and fibrosis over time. This model is important for studying metabolic disturbances and renal dysfunction in CKD, providing a tool to assess the efficacy of drugs designed to halt or reverse kidney fibrosis in clinical settings.
5/6 Nephrectomy Animal Model
5/6 nephrectomy involves removing a large portion of kidney mass, leading to progressive renal dysfunction and fibrosis. This model simulates the pathophysiology of CKD and end-stage renal disease, providing a valuable tool for investigating the mechanisms of renal fibrosis, glomerular injury, and tubular damage. It is often used to evaluate the therapeutic potential of anti-fibrotic agents in the context of advanced kidney disease.
2/3 and UNx
bleomycin administration
Treatment
(Options: IP, IV, SC, IM)
Terminate study/harvest organs
(56 days post UNx)
Data analysis
(Serum chemistry, urine proteinuria, kidney hydroxyproline histopathology
Draft/final report
