Transcriptomics: a Solution for Renal Osteodystrophy?

Martin, Aline; David, Véronique

doi:10.1007/s11914-020-00583-6

Cited by 5 publications

(3 citation statements)

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“…We previously called 'mineralostat' the process of sensing and regulating minerals, to maintain homeostasis or return to homeostasis following stress [54]. This mineralostat is highly relevant and of paramount interest in medical research because it contains the elusive mechanism that fails in chronic diseases such as CKD leading to profound alterations in mineral metabolism and eventually skeletal abnormalities [54,55]. Thus, iron metabolism could be part of the 'mineralostat' designation of the mechanisms leading to increased FGF23 production and opens a number of questions to understand how and why phosphate loading and iron deficiency would both regulate the same hormone, if in turn this hormone regulates only phosphate excretion and vitamin D metabolism [56][57][58].…”

Section: C-terminal Fibroblast Growth Factor 23 Is a Novel Bioactive ...mentioning

confidence: 99%

Fibroblast growth factor 23 is pumping iron: C-terminal-fibroblast growth factor 23 cleaved peptide and its function in iron metabolism

Courbon,

David

2024

Current Opinion in Nephrology &Amp; Hypertension

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Purpose of the review Iron deficiency regulates the production of the bone-derived phosphaturic hormone fibroblast growth factor 23 (FGF23) but also its cleavage, to generate both intact (iFGF23) and C-terminal (Cter)-FGF23 peptides. Novel studies demonstrate that independently of the phosphaturic effects of iFGF23, Cter-FGF23 peptides play an important role in the regulation of systemic iron homeostasis. This review describes the complex interplay between iron metabolism and FGF23 biology. Recent findings C-terminal (Cter) FGF23 peptides antagonize inflammation-induced hypoferremia to maintain a pool of bioavailable iron in the circulation. A key mechanism proposed is the down-regulation of the iron-regulating hormone hepcidin by Cter-FGF23. Summary In this manuscript, we discuss how FGF23 is produced and cleaved in response to iron deficiency, and the principal functions of cleaved C-terminal FGF23 peptides. We also review possible implications anemia of chronic kidney disease (CKD).

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Section: C-terminal Fibroblast Growth Factor 23 Is a Novel Bioactive ...mentioning

confidence: 99%

Fibroblast growth factor 23 is pumping iron: C-terminal-fibroblast growth factor 23 cleaved peptide and its function in iron metabolism

Courbon,

David

2024

Current Opinion in Nephrology &Amp; Hypertension

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“…Recent advances in transcriptomics now permit single cell and single nuclei analyses of bone cells [46][47][48]. State-of-the art methods in single cell and single nuclei RNA sequencing of bone will lead to major advances in our understanding of ROD pathogenesis and inform the development of targeted disease-modifying and curative strategies.…”

Section: Andandmentioning

confidence: 99%

Renal osteodystrophy: something old, something new, something needed

David,

Salusky,

Malluche

et al. 2023

Current Opinion in Nephrology &Amp; Hypertension

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Purpose of review Renal osteodystrophy (ROD) is a complex disorder of bone metabolism that affects virtually all adults and children with chronic kidney disease (CKD). ROD is associated with adverse clinical outcomes including bone loss, mineralization and turnover abnormalities, skeletal deformities, fractures, cardiovascular events, and death. Despite current therapies, fracture incidence is 2-fold to 100-fold higher in adults and 2-fold to 3-fold higher in children when compared to without CKD. Limited knowledge of ROD pathogenesis, due to the lack of patient-derived large-scale multimodal datasets, impedes development of therapeutics aimed at reducing morbidity and mortality of CKD patients. The purpose of the review is to define the much needed infrastructure for the advancement of RDO treatment. Recent findings Recently, we created a large-scale data and tissue biorepository integrating clinical, bone quality, transcriptomic, and epigenomic data along with stored urine, blood, and bone samples. This database will provide the underpinnings for future research endeavors leading to the elucidation and characterization of the pathogenesis of ROD in CKD patients with and without dialysis. Summary The availability of an open-access NIH-funded resource that shares bone-tissue-based information obtained from patients with ROD with the broad scientific community represents a critical step in the process of discovering new information regarding unrecognized bone changes that have severe clinical complications. This will facilitate future high-impact hypothesis-driven research to redefine our understanding of ROD pathogenesis and pathophysiology and inform the development of disease-modifying and prevention strategies

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“…Transcriptomics, representing the analysis of messenger ribonucleic acids (mRNAs) and small noncoding ribonucleic acids such as microribonucleic acids (miRNAs) by quantitative polymerase chain reaction (qPCR), microarray or RNA sequencing, from bone tissue or single bone cells may help to unravel pathophysiological mechanisms and to identify clinically relevant biomarkers ( Martin and David, 2020 ).…”

Section: Introductionmentioning

confidence: 99%