The Role of Fibroblast Growth Factor 19 Subfamily in Different Populations Suffering From Osteoporosis

Yu, Xiawen; Xia, Yue; Jia, Junjing; Yuan, Guoyue

doi:10.3389/fendo.2022.830022

Front. Endocrinol.

2022

DOI: 10.3389/fendo.2022.830022

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The Role of Fibroblast Growth Factor 19 Subfamily in Different Populations Suffering From Osteoporosis

Xiawen Yu

Yue Xia

Junjing Jia

et al.

Abstract: Fibroblast growth factor (FGF) 19 subfamily, also known as endocrine fibroblast growth factors (FGFs), is a newly discovered metabolic regulator, including FGF19, FGF21 and FGF23. They play significant roles in maintaining systemic homeostasis, regulating the balance of bile acid and glucolipid metabolism in humans. Osteoporosis is a chronic disease, especially in the current status of aging population, osteoporosis is the most prominent chronic bone disease, leading to multiple complications and a significant… Show more

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Cited by 3 publications

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Role of signaling pathways in age-related orthopedic diseases: focus on the fibroblast growth factor family

Li,

Zhang,

Yuan

et al. 2024

Military Med Res

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Fibroblast growth factor (FGF) signaling encompasses a multitude of functions, including regulation of cell proliferation, differentiation, morphogenesis, and patterning. FGFs and their receptors (FGFR) are crucial for adult tissue repair processes. Aberrant FGF signal transduction is associated with various pathological conditions such as cartilage damage, bone loss, muscle reduction, and other core pathological changes observed in orthopedic degenerative diseases like osteoarthritis (OA), intervertebral disc degeneration (IVDD), osteoporosis (OP), and sarcopenia. In OA and IVDD pathologies specifically, FGF1, FGF2, FGF8, FGF9, FGF18, FGF21, and FGF23 regulate the synthesis, catabolism, and ossification of cartilage tissue. Additionally, the dysregulation of FGFR expression (FGFR1 and FGFR3) promotes the pathological process of cartilage degradation. In OP and sarcopenia, endocrine-derived FGFs (FGF19, FGF21, and FGF23) modulate bone mineral synthesis and decomposition as well as muscle tissues. FGF2 and other FGFs also exert regulatory roles. A growing body of research has focused on understanding the implications of FGF signaling in orthopedic degeneration. Moreover, an increasing number of potential targets within the FGF signaling have been identified, such as FGF9, FGF18, and FGF23. However, it should be noted that most of these discoveries are still in the experimental stage, and further studies are needed before clinical application can be considered. Presently, this review aims to document the association between the FGF signaling pathway and the development and progression of orthopedic diseases. Besides, current therapeutic strategies targeting the FGF signaling pathway to prevent and treat orthopedic degeneration will be evaluated.

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Role of signaling pathways in age-related orthopedic diseases: focus on the fibroblast growth factor family

Li,

Zhang,

Yuan

et al. 2024

Military Med Res

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Exploring the Role of Hormones and Cytokines in Osteoporosis Development

Umur,

Bulut,

Yiğit

et al. 2024

Biomedicines

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The disease of osteoporosis is characterized by impaired bone structure and an increased risk of fractures. There is a significant impact of cytokines and hormones on bone homeostasis and the diagnosis of osteoporosis. As defined by the World Health Organization (WHO), osteoporosis is defined as having a bone mineral density (BMD) that is 2.5 standard deviations (SD) or more below the average for young and healthy women (T score < −2.5 SD). Cytokines and hormones, particularly in the remodeling of bone between osteoclasts and osteoblasts, control the differentiation and activation of bone cells through cytokine networks and signaling pathways like the nuclear factor kappa-B ligand (RANKL)/the receptor of RANKL (RANK)/osteoprotegerin (OPG) axis, while estrogen, parathyroid hormones, testosterone, and calcitonin influence bone density and play significant roles in the treatment of osteoporosis. This review aims to examine the roles of cytokines and hormones in the pathophysiology of osteoporosis, evaluating current diagnostic methods, and highlighting new technologies that could help for early detection and treatment of osteoporosis.

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Effects of Burosumab Treatment on Two Siblings with X-Linked Hypophosphatemia. Case Report and Literature Review

Jurcă

Iuhas

Kozma

et al. 2022

Genes

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X-linked hypophosphatemia (XLH) or vitamin D-resistant rickets (MIM#307800), is a monogenic disorder with X-linked inheritance. It is caused by mutations present in the Phosphate Regulating Endopeptidase Homolog X-Linked (PHEX) gene responsible for the degradation of the bone-derived hormone fibroblast growth factor 23 (FGF23) into inactive fragments, but the entire mechanism is currently unclear. The inactivation of the gene prevents the degradation of FGF23, causing increased levels of FGF23, which leads to decreased tubular reabsorbtion of phosphorus. Clinical aspects are growth delay, limb deformities, bone pain, osteomalacia, dental anomalies, and enthesopathy. Laboratory evaluation shows hypophosphatemia, elevated alkaline phosphatase (ALP), and normal serum calcium levels, whereas parathormone (PTH) may be normal or increased and FGF23 greatly increased. Conventional treatment consists of administration of oral phosphate and calcitriol. Treatment with Burosumab, a monoclonal antibody that binds to FGF23, reducing its activity, was approved in 2018. Methods. We describe a case of two siblings, a girl and a boy, diagnosed with XLH, monitored by the Genetic Department of the County Emergency Clinical Hospital since 2019. The clinical picture is suggestive for XLH, both siblings exhibiting short stature, lower limb curvature, bone pain, marked walking weakness, and fatigue. Radiological aspects showed marked deformity of the lower limbs: genu varum in the girl, genu varum and valgum in the boy. Laboratory investigations showed hypophosphathemia, hyperphosphaturia, elevated ALP, normal PTH, and highly increased FGF23 in both. DNA analysis performed on the two siblings revealed a nonsense mutation in exone 5 of the PHEX gene: NM_000444.6(PHEX):c.565C > T (p.Gln189Ter). Results. At the age of 13½ on 7 June 2021, the two children started treatment with Burosumab in therapeutic doses and were monitored clinically and biochemically at regular intervals according to the protocol established by the Endocrinology Commission of the Romanian Health Ministry. Conclusions. The first results of the Burosumab treatment in the two siblings are extremely encouraging and suggest a favorable long-term evolution under this treatment.

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The Role of Fibroblast Growth Factor 19 Subfamily in Different Populations Suffering From Osteoporosis

Cited by 3 publications

References 70 publications

Role of signaling pathways in age-related orthopedic diseases: focus on the fibroblast growth factor family

Role of signaling pathways in age-related orthopedic diseases: focus on the fibroblast growth factor family

Exploring the Role of Hormones and Cytokines in Osteoporosis Development

Effects of Burosumab Treatment on Two Siblings with X-Linked Hypophosphatemia. Case Report and Literature Review

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