Transcriptomics: a Solution for Renal Osteodystrophy?
- PMID: 32222893
- PMCID: PMC8191338
- DOI: 10.1007/s11914-020-00583-6
Transcriptomics: a Solution for Renal Osteodystrophy?
Abstract
Purpose of review: The molecular mechanisms of the bone disease associated with chronic kidney disease (CKD), called renal osteodystrophy (ROD), are poorly understood. New transcriptomics technologies may provide clinically relevant insights into the pathogenesis of ROD. This review summarizes current progress and limitations in the study and treatment of ROD, and in transcriptomics analyses of skeletal tissues.
Recent findings: ROD is characterized by poor bone quality and strength leading to increased risk of fracture. Recent studies indicate permanent alterations in bone cell populations during ROD. Single-cell transcriptomics analyses, successful at identifying specialized cell subpopulations in bone, have not yet been performed in ROD. ROD is a widespread poorly understood bone disease with limited treatment options. Transcriptomics analyses of bone are needed to identify the bone cell subtypes and their role in the pathogenesis of ROD, and to develop adequate diagnosis and treatment strategies.
Keywords: Bone and mineral metabolism; Bulk RNA sequencing; Chronic kidney disease; Renal osteodystrophy; Single-cell RNA sequencing; Transcriptomics.
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References
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Dussold C, Gerber C, White S, Wang X, Qi L, Francis C, et al. DMP1 prevents osteocyte alterations, FGF23 elevation and left ventricular hypertrophy in mice with chronic kidney disease. Bone research. 2019;7:12.
** This study shows that osteocyte secretion of DMP1 is reduced in the bone of mice with CKD, and that DMP1 repletion reverses ROD.
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Pereira RC, Salusky IB, Roschger P, Klaushofer K, Yadin O, Freymiller EG, et al. Impaired osteocyte maturation in the pathogenesis of renal osteodystrophy. Kidney international. 2018;94(5):1002–12.
** This study shows that osteoblast and osteocyte maturation is altered in cell cultures isolated from bone biopsies of pediatric patients with ROD, suggesting that molecular changes affecting bone cells are independent of systemic perturbations.
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