Bone and bone derived factors in kidney disease
Purpose of review: Mineral and bone disorder (MBD) is a prevalent complication in chronic kidney disease (CKD), significantly impacting overall health with multifaceted implications including fractures, cardiovascular events, and mortality. Despite its pervasive nature, effective treatments for CKD-...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2024-03-01
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| Series: | Frontiers in Physiology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fphys.2024.1356069/full |
| _version_ | 1797289477882773504 |
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| author | Petra Simic Petra Simic |
| author_facet | Petra Simic Petra Simic |
| author_sort | Petra Simic |
| collection | DOAJ |
| description | Purpose of review: Mineral and bone disorder (MBD) is a prevalent complication in chronic kidney disease (CKD), significantly impacting overall health with multifaceted implications including fractures, cardiovascular events, and mortality. Despite its pervasive nature, effective treatments for CKD-MBD are lacking, emphasizing the urgency to advance understanding and therapeutic interventions. Bone metabolism intricacies, influenced by factors like 1,25 dihydroxy vitamin D, parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF23), along with intrinsic osseous mechanisms, play pivotal roles in CKD. Skeletal abnormalities precede hormonal changes, persisting even with normalized systemic mineral parameters, necessitating a comprehensive approach to address both aspects.Recent findings: In this review, we explore novel pathways involved in the regulation of systemic mineral bone disease factors, specifically examining anemia, inflammation, and metabolic pathways. Special emphasis is placed on internal bone mechanisms, such as hepatocyte nuclear factor 4α, transforming growth factor-β1, and sclerostin, which play crucial roles in the progression of renal osteodystrophy.Summary: Despite advancements, effective treatments addressing CKD-MBD morbidity and mortality are lacking, necessitating ongoing research for novel therapeutic targets. |
| first_indexed | 2024-03-07T19:05:33Z |
| format | Article |
| id | doaj.art-a3b8a68b2d4d483987b27c61fa643d7c |
| institution | Directory Open Access Journal |
| issn | 1664-042X |
| language | English |
| last_indexed | 2024-03-07T19:05:33Z |
| publishDate | 2024-03-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Physiology |
| spelling | doaj.art-a3b8a68b2d4d483987b27c61fa643d7c2024-03-01T09:21:32ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2024-03-011510.3389/fphys.2024.13560691356069Bone and bone derived factors in kidney diseasePetra Simic0Petra Simic1Division of Nephrology, Massachusetts General Hospital, Boston, MA, United StatesEndocrine Unit, Massachusetts General Hospital, Boston, MA, United StatesPurpose of review: Mineral and bone disorder (MBD) is a prevalent complication in chronic kidney disease (CKD), significantly impacting overall health with multifaceted implications including fractures, cardiovascular events, and mortality. Despite its pervasive nature, effective treatments for CKD-MBD are lacking, emphasizing the urgency to advance understanding and therapeutic interventions. Bone metabolism intricacies, influenced by factors like 1,25 dihydroxy vitamin D, parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF23), along with intrinsic osseous mechanisms, play pivotal roles in CKD. Skeletal abnormalities precede hormonal changes, persisting even with normalized systemic mineral parameters, necessitating a comprehensive approach to address both aspects.Recent findings: In this review, we explore novel pathways involved in the regulation of systemic mineral bone disease factors, specifically examining anemia, inflammation, and metabolic pathways. Special emphasis is placed on internal bone mechanisms, such as hepatocyte nuclear factor 4α, transforming growth factor-β1, and sclerostin, which play crucial roles in the progression of renal osteodystrophy.Summary: Despite advancements, effective treatments addressing CKD-MBD morbidity and mortality are lacking, necessitating ongoing research for novel therapeutic targets.https://www.frontiersin.org/articles/10.3389/fphys.2024.1356069/fullrenal osteodystrophyCKD-MBDmineral and bone disorderCKDFGF23 = fibroblast growth factor 23 |
| spellingShingle | Petra Simic Petra Simic Bone and bone derived factors in kidney disease Frontiers in Physiology renal osteodystrophy CKD-MBD mineral and bone disorder CKD FGF23 = fibroblast growth factor 23 |
| title | Bone and bone derived factors in kidney disease |
| title_full | Bone and bone derived factors in kidney disease |
| title_fullStr | Bone and bone derived factors in kidney disease |
| title_full_unstemmed | Bone and bone derived factors in kidney disease |
| title_short | Bone and bone derived factors in kidney disease |
| title_sort | bone and bone derived factors in kidney disease |
| topic | renal osteodystrophy CKD-MBD mineral and bone disorder CKD FGF23 = fibroblast growth factor 23 |
| url | https://www.frontiersin.org/articles/10.3389/fphys.2024.1356069/full |
| work_keys_str_mv | AT petrasimic boneandbonederivedfactorsinkidneydisease AT petrasimic boneandbonederivedfactorsinkidneydisease |