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Mouse Models of Mineral Bone Disorders Associated with Chronic Kidney Disease
Ariane Zaloszyc1,2, Julie Bernardor3,4,5, Justine Bacchetta5,6,7,8
1Service de Pédiatrie 1, Hôpital de Hautepierre, Hôpitaux Universitaires de Strasbourg, 67000 Strasbourg, France.
Abstract:
Patients with chronic kidney disease (CKD) inevitably develop mineral and bone disorders (CKD-MBD), which negatively impact their survival and quality of life. For a better understanding of underlying pathophysiology and identification of novel therapeutic approaches, mouse models are essential. CKD can be induced by surgical reduction of a functional kidney mass, by nephrotoxic compounds and by genetic engineering specifically interfering with kidney development. These models develop a large range of bone diseases, recapitulating different types of human CKD-MBD and associated sequelae, including vascular calcifications. Bones are usually studied by quantitative histomorphometry, immunohistochemistry and micro-CT, but alternative strategies have emerged, such as longitudinal in vivo osteoblast activity quantification by tracer scintigraphy. The results gained from the CKD-MBD mouse models are consistent with clinical observations and have provided significant knowledge on specific pathomechanisms, bone properties and potential novel therapeutic strategies. This review discusses available mouse models to study bone disease in CKD.
Insights
Mouse models are crucial for understanding chronic kidney disease mineral and bone disorders (CKD-MBD). These models help identify new therapies for CKD-MBD, improving patient survival and quality of life.
Area of Science:
- Nephrology
- Orthopedics
- Translational Medicine
Background:
- Chronic kidney disease (CKD) invariably leads to mineral and bone disorders (CKD-MBD), significantly impacting patient survival and quality of life.
- Understanding the pathophysiology of CKD-MBD is critical for developing effective therapeutic strategies.
Purpose of the Study:
- To review and discuss available mouse models for studying bone disease in CKD.
- To highlight the utility of these models in elucidating CKD-MBD pathophysiology and identifying novel therapeutic targets.
Main Methods:
- CKD induction via surgical reduction of kidney mass, nephrotoxic compounds, or genetic engineering.
- Characterization of bone diseases and vascular calcifications in CKD mouse models.
- Utilizing techniques like histomorphometry, micro-CT, and in vivo osteoblast activity quantification.
Main Results:
- CKD mouse models recapitulate a spectrum of human CKD-MBD, including vascular calcifications.
- Data from these models align with clinical observations, advancing knowledge of pathomechanisms.
- These models facilitate the exploration of potential novel therapeutic strategies.
Conclusions:
- Mouse models are indispensable tools for investigating bone disease in CKD.
- They provide valuable insights into CKD-MBD, aiding in the development of improved treatments.
- Continued use of these models is essential for enhancing patient outcomes in CKD.
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