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Although subsets of patients with lung squamous cell carcinoma (LSCC) benefit from immunotherapy, there are few effective molecularly targeted treatments for LSCC. Fibroblast growth factor receptor (FGFR) inhibitors provide a therapeutic option for patients with LSCC harboring FGFR aberrations, but their therapeutic efficacy has been limited to date. In this issue of the JCI, Malchers et al. identified tail-to-tail rearrangements, either within or near FGFR1, that are associated with FGFR1 dependency and sensitivity to FGFR inhibition in LSCC. These results may help improve the selection of patients with LSCC who are most likely to benefit from treatment with FGFR inhibitors., Treatment of LSCC remains an unmet need Lung squamous cell carcinoma (LSCC) is the second most common subtype of non-small cell lung cancer (NSCLC) after lung adenocarcinoma. In the past [...]

Adipose tissue browning is a physiological process that increases energy expenditure and may combat against obesity and its related risk factors. Fibroblast growth factor 21 (FGF21) and irisin, hormones affected by exercise that also affect adipose tissue browning, have not been widely studied with regard to exercise type and duration. This study compared the effect of high-intensity interval training (HIIT) and high-intensity resistance training (HIRT) on irisin and FGF21 in men living with overweight and obesity. After completing a training program three times weekly for 8 weeks, participants' serum levels of irisin and FGF21 were significantly increased in the HIIT and HIRT groups compared with the control group (p < 0.05). Additionally, body fat percentage and body weight in both training groups were significantly reduced in comparison with the control group (p < 0.05). Thus, HIIT and HIRT programs may be used as a feasible modality to promote favourable changes in body composition and irisin and FGF21, factors critical for browning white adipose tissue in men living with overweight and obesity. Key words: adipose tissue, fibroblast growth factor 21, interval training, irisin, obesity, resistance training Le brunissement du tissu adipeux est un processus physiologique, qui entraine une augmentation des depenses energetiques et qui pourrait permettre de contrer l'obesite et les facteurs de risque qui y sont lies. Le facteur de croissance des fibroblastes 21 (ou FGF21 pour << fibroblast growth factor 21 >>) et l'irisine, des hormones touchees par l'exercice physique qui modifient aussi le brunissement du tissu adipeux, n'ont pas ete largement etudies quant au type d'exercice physique et a sa duree. Cette etude consistait a comparer l'effet de l'entrainement fractionne de haute intensite (ou HIIT pour << high-intensity interval training >>) et de l'entrainement contre resistance de haute intensite (ou HIRT pour << high-intensity resistance training >>) sur l'irisine et le FGF21 chez des hommes aux prises avec un surpoids et de l'obesite. Apres avoir termine un programme d'entrainement physique trois fois par semaine pendant huit semaines, on observait chez les participants une augmentation nettement plus marquee des taux seriques d'irisine et de FGF21 dans les groupes HIIT et HIRT que chez les temoins (p < 0,05). De plus, le pourcentage de tissu adipeux corporel et la masse corporelle diminuaient nettement plus dans les deux groupes d'entrainement que chez les temoins (p < 0,05). Par consequent, les programmes de HIIT et de HIRT pourraient etre utilises comme modalite realisable en vue de favoriser des modifications favorables quant a la composition de l'organisme, de meme qu'en matiere d'irisine avec de FGF21, des facteurs cruciaux pour le brunissement du tissu adipeux blanc chez les hommes aux prises avec un surpoids et de l'obesite. [Traduit par la Redaction] Mots-cles : tissu adipeux, facteur de croissance des fibroblastes 21, entrainement fractionne, irisine, obesite, entrainement contre resistance, Introduction Obesity as a multifactorial disease has adverse effects on health and economic outcomes (Bray et al. 2018). Previous studies have reported that increased adipose tissue mass as the main [...]

Cutaneous skeletal hypophosphatemia syndrome (CSHS) is a mosaic RA Sopathy characterized by the association of dysplastic skeletal lesions, congenital skin nevi of epidermal and/or melanocytic origin, and FGF23-mediated hypophosphatemia. The primary physiological source of circulating FGF23 is bone cells. However, several reports have suggested skin lesions as the source of excess FGF23 in CSHS. Consequently, without convincing evidence of efficacy, many patients with CSHS have undergone painful removal of cutaneous lesions in an effort to normalize blood phosphate levels. This study aims to elucidate whether the source of FGF23 excess in CSHS is RAS mutation-bearing bone or skin lesions. Toward this end, we analyzed the expression and activity of Fgf23 in two mouse models expressing similar HRAS/Hras activating mutations in a mosaic-like fashion in either bone or epidermal tissue. We found that HRAS hyperactivity in bone, not skin, caused excess of bioactive intact FGF23, hypophosphatemia, and osteomalacia. Our findings support RAS- mutated dysplastic bone as the primary source of physiologically active FGF23 excess in patients with CSHS. This evidence informs the care of patients with CSHS, arguing against the practice of nevi removal to decrease circulating, physiologically active FGF23., Introduction Cutaneous skeletal hypophosphatemia syndrome (CSHS) is characterized by the association of dysplastic skeletal lesions, congenital skin nevi of epidermal and/or melanocytic origin (including epidermal nevi [EN], giant congenital melanocytic [...]

Background Children living with HIV frequently show high plasma levels of fibroblast growth factor-2 (FGF-2/bFGF). FGF-2 accelerates the progression of several experimental kidney diseases; however, the role of circulating FGF-2 in childhood HIV-chronic kidney diseases (HIV-CKDs) is unknown. We carried out this study to determine whether high plasma FGF-2 levels were associated with the development of HIV-CKDs in children. Methods The plasma and urine FGF-2 levels were measured in 84 children (< 12 years of age) living with HIV during the pre-modern antiretroviral era, and followed for at least 3 years to determine the prevalence of proteinuria and HIV-CKDs. We also assessed the distribution of the kidney FGF-2 binding sites by autoradiography and Alcian blue staining, and explored potential mechanisms by which circulating FGF-2 may precipitate HIV-CKDs in cultured kidney epithelial and mononuclear cells derived from children with HIV-CKDs. Results High plasma FGF-2 levels were associated with a high viral load. Thirteen children (~ 15%) developed HIV-CKDs and showed a large reservoir of FGF-2 low-affinity binding sites in the kidney, which can facilitate the recruitment of circulating FGF-2. Children with high plasma and urine FGF-2 levels had 73-fold increased odds (95% CI 9-791) of having HIV-CKDs relative to those with normal FGF-2 values. FGF-2 induced the proliferation and decreased the expression of APOL-1 mRNA in podocytes, and increased the attachment and survival of infected mononuclear cells cultured from children with HIV-CKDs. Conclusions High plasma FGF-2 levels appear to be an additional risk factor for developing progressive childhood HIV-CKDs. Graphical abstract, Author(s): Patricio E. Ray [sup.1] , Jinliang Li [sup.2] [sup.3] , Jharna R. Das [sup.2] [sup.3] , Jing Yu [sup.1] Author Affiliations: (1) grid.27755.32, 0000 0000 9136 933X, Child Health [...]

Background In pediatric kidney transplant recipients, anemia is common and oftentimes multifactorial. Hemoglobin concentrations may be affected by traditional factors, such as kidney function and iron status, as well as novel parameters, such as fibroblast growth factor 23 (FGF23). Methods Here, we evaluated associations among erythropoietic, iron-related, and FGF23 parameters in a cohort of pediatric kidney transplant recipients, hypothesizing that multiple factors are associated with hemoglobin concentrations. Results In a cross-sectional analysis of 59 pediatric kidney transplant recipients (median (interquartile range) age 16.3 (13.5, 18.6) years, median estimated glomerular filtration rate (eGFR) 67 (54, 87) ml/min/1.73 m.sup.2), the median age-related hemoglobin standard deviation score (SDS) was -2.1 (-3.3, -1.1). Hemoglobin SDS was positively associated with eGFR and calcium, and was inversely associated with erythropoietin (EPO), mycophenolate dose, and total, but not intact, FGF23. In multivariable analysis, total FGF23 remained inversely associated with hemoglobin SDS, independent of eGFR, iron parameters, EPO, and inflammatory markers, suggesting a novel FGF23-hemoglobin association in pediatric kidney transplant patients. In a subset of patients with repeat measurements, only delta hepcidin was inversely associated with delta hemoglobin SDS. Also, delta EPO positively correlated with delta erythroferrone (ERFE), and delta ERFE inversely correlated with delta hepcidin, suggesting a possible physiologic role for the EPO-ERFE-hepcidin axis in the setting of chronic kidney disease (CKD). Conclusion Our study provides further insight into factors potentially associated with erythropoiesis in pediatric kidney transplant recipients. Graphical abstract, Author(s): Blair Limm-Chan [sup.1] , Katherine Wesseling-Perry [sup.1] , Meghan H. Pearl [sup.1] , Grace Jung [sup.2] , Eileen Tsai-Chambers [sup.3] , Patricia L. Weng [sup.1] , Mark R. Hanudel [...]

Author(s): Judith Sebestyen VanSickle [sup.1] , Tarak Srivastava [sup.1] , Penny Monachino [sup.1] , Uri S. Alon [sup.1] Author Affiliations: (1) grid.266756.6, 0000 0001 2179 926X, Bone and Mineral Disorders [...]

Background Primary hypophosphatemic syndromes are a heterogeneous group of rare diseases. In recent years, fibroblast growth factor 23 (FGF23) has been postulated as a useful tool for differential diagnosis of hypophosphatemic rickets characterized by impaired renal phosphate reabsorption. This study aimed to investigate the utility of FGF23 to discriminate between X-linked hypophosphatemic rickets (XLH), an FGF23-driven disease, from other causes of renal phosphate wasting such as Fanconi syndrome (FS), a generalized dysfunction of the proximal tubule unrelated to FGF23. Methods Circulating levels of intact FGF23 (iFGF23) were measured in nine children with XLH receiving conventional therapy (six girls, mean ± SD age 10.8 ± 6.7 years) and nine children with secondary FS (four girls, mean ± SD age 9.9 ± 5.2 years), using an automated chemiluminescent immunoassay. Phosphate, calcium, creatinine, estimated glomerular filtration rate (eGFR), intact parathormone (iPTH), and urinary parameters were evaluated simultaneously. Maximum renal tubular threshold for phosphate reabsorption (TmP/GFR) was also estimated. Results Plasma iFGF23 concentrations in patients with XLH were significantly higher than those in the SF group: 146.2 ± 69.2 ng/L vs. 29.5 ± 15.0 ng/L (p < 0.001). Remarkably, we did not observe an overlap between XLH and FS patients. Significant hypophosphatemia (2.55 ± 0.50 mg/dL) and secondary hyperparathyroidism (iPTH 109.4 ± 58.1 ng/mL) were present in XLH patients, while FS patients showed modest hypophosphatemia (3.97 ± 0.68 mg/dL), higher TmP/GFR compared with XLH, lower eGFR and hypercalciuria. Conclusions This study supports the value of measuring FGF23 levels as a useful tool to exclude XLH in patients with increased phosphate wasting of kidney origin., Author(s): Marina Giralt [sup.1] , Sara Chocron [sup.2] , Roser Ferrer [sup.1] , Gema Ariceta [sup.3] Author Affiliations: (1) grid.411083.f, 0000 0001 0675 8654, Department of Biochemistry, Vall d'Hebron University [...]

Demyelination in the central nervous system (CNS) leads to severe neurological deficits that can be partially reversed by spontaneous remyelination. Because the CNS is isolated from the peripheral milieu by the blood-brain barrier, remyelination is thought to be controlled by the CNS microenvironment. However, in this work we found that factors derived from peripheral tissue leak into the CNS after injury and promote remyelination in a murine model of toxin-induced demyelination. Mechanistically, leakage of circulating fibroblast growth factor 21 (FGF21), which is predominantly expressed by the pancreas, drives proliferation of oligodendrocyte precursor cells (OPCs) through interactions with [beta]-klotho, an essential coreceptor of FGF21. We further confirmed that human OPCs expressed [beta]-klotho and proliferated in response to FGF21 in vitro. Vascular barrier disruption is a common feature of many CNS disorders; thus, our findings reveal a potentially important role for the peripheral milieu in promoting CNS regeneration., Introduction Central nervous system (CNS) damage, a hallmark of many CNS disorders, is causatively associated with severe neurological deficits in motor, sensory, cognitive, and other functions (1). Because damaged CNS [...]

Type 2 diabetes (T2D) is among the most common and costly disorders worldwide (1). The goal of current medical management for T2D is to transiently ameliorate hyperglycemia through daily dosing of one or more antidiabetic drugs. Hypoglycemia and weight gain are common side effects of therapy, and sustained disease remission is not obtainable with nonsurgical approaches. On the basis of the potent glucose-lowering response elicited by activation of brain fibroblast growth factor (FGF) receptors (2-4), we explored the antidiabetic efficacy of centrally administered FGF1, which, unlike other FGF peptides, activates all FGF receptor subtypes (5). We report that a single intracerebroventricular injection of FGF1 at a dose one-tenth of that needed for antidiabetic efficacy following peripheral injection induces sustained diabetes remission in both mouse and rat models of T2D. This antidiabetic effect is not secondary to weight loss, does not increase the risk of hypoglycemia, and involves a novel and incompletely understood mechanism for increasing glucose clearance from the bloodstream. We conclude that the brain has an inherent potential to induce diabetes remission and that brain FGF receptors are potential pharmacological targets for achieving this goal., Growing evidence points to the brain as a potential target for the treatment of T2D (6,7). In rodent models of T2D, hyperglycemia can be ameliorated transiently by either systemic or [...]

Achondroplasia (ACH) is the most frequent form of dwarfism and is caused by gain-of-function mutations in the fibroblast growth factor receptor 3-encoding (FGFR3-encoding) gene. Although potential therapeutic strategies for ACH, which aim to reduce excessive FGFR3 activation, have emerged over many years, the use of tyrosine kinase inhibitor (TKI) to counteract FGFR3 hyperactivity has yet to be evaluated. Here, we have reported that the pan-FGFR TKI, NVP-BGJ398, reduces FGFR3 phosphorylation and corrects the abnormal femoral growth plate and calvaria in organ cultures from embryos of the [Fgfr3.sup.Y367C/+] mouse model of ACH. Moreover, we demonstrated that a low dose of NVP-BGJ398, injected subcutaneously, was able to penetrate into the growth plate of [Fgfr3.sup.Y367C/+] mice and modify its organization. Improvements to the axial and appendicular skeletons were noticeable after 10 days of treatment and were more extensive after 15 days of treatment that started from postnatal day 1. Low-dose NVP-BGJ398 treatment reduced intervertebral disc defects of lumbar vertebrae, loss of synchondroses, and foramen-magnum shape anomalies. NVP-BGJ398 inhibited FGFR3 downstream signaling pathways, including MAPK, SOX9, STAT1, and PLCγ, in the growth plates of [Fgfr3.sup.Y367C/+] mice and in cultured chondrocyte models of ACH. Together, our data demonstrate that NVP-BGJ398 corrects pathological hallmarks of ACH and support TKIs as a potential therapeutic approach for ACH., Introduction Achondroplasia (ACH) is the most common form of dwarfism, which occurs with an estimated prevalence of between 1/16,000 and 1/25,000 live births (1, 2). ACH patients are characterized by [...]

Overexpression of FGF23 results in hypophosphatemic rickets, which is characterized by renal phosphate wasting, inappropriately low circulating levels of the active form of vitamin D, and skeletal abnormalities. The precise mechanisms of how excess FGF23 leads to hypophosphatemic rickets are not clear. In this issue of theJCI, Bai and colleagues demonstrate that deletion or inhibition of CYP24A1, which initiates degradation of the active form of vitamin D, ameliorates skeletal abnormalities in two mouse models of hypophosphatemic rickets. While this work supports an important role for excess CYP24A1 activity in the pathogenesis of FGF23mediated hypophosphatemic rickets, more work will need to be done before CYP24A1 inhibition can be integrated into the management of patients living with these diseases., Precise regulation of FGF23 is required for bone health Just the right amount of FGF23 is required to maintain healthy bone and mineral metabolism. FGF23 deficiency results in tumoral calcinosis, [...]

CYP24A1 (hereafter referred to as CYP24) enzymatic activity is pivotal in the inactivation of vitamin D metabolites. Basal renal and extrarenal CYP24 is usually low but is highly induced by its substrate 1,25-dihydroxyvitamin D. Unbalanced high and/or long-lasting CYP24 expression has been proposed to underlie diseases like chronic kidney disease, cancers, and psoriasis that otherwise should favorably respond to supplemental vitamin D. Using genetically modified mice, we have shown that renal phosphate wasting hypophosphatemic states arising from high levels of fibroblast growth factor 23 (FGF23) are also associated with increased renal Cyp24 expression, suggesting that elevated CYP24 activity is pivotal to the pathophysiology of these disorders. We therefore crossed 2 mouse strains, each with distinct etiology for high levels of circulating FGF23, onto a Cyp24-null background. Specifically, we evaluated Cyp24 deficiency in Hyp mice, the murine homolog of X-linked dominant hypophosphatemic rickets, and transgenic mice that overexpress a mutant FGF23 ([FGF23.sup.R176Q]) that is associated with the autosomal dominant form of hypophosphatemic rickets. Loss of Cyp24 in these murine models of human disease resulted in near-complete recovery of rachitic/osteomalacic bony abnormalities in the absence of any improvement in the serum biochemical profile. Moreover, treatment of Hyp and [FGF23.sup.R1760]-transgenic mice with the CYP24 inhibitor CTA102 also ameliorated their rachitic bones. Our results link CYP24 activity to the pathophysiology of FGF23-dependent renal phosphate wasting states and implicate pharmacologic CYP24 inhibition as a therapeutic adjunct for their treatment., Introduction Fibroblast growth factor 23 (FGF23) is a bone-derived humoral factor underlying the etiology of several inherited and acquired renal phosphate wasting diseases (1, 2). It is highly expressed in [...]

Background Emerging data in chronic kidney disease (CKD) patients suggest that iron deficiency and higher circulating levels of erythropoietin (EPO) stimulate the expression and concomitant cleavage of the osteocyte-derived, phosphate-regulating hormone fibroblast growth factor 23 (FGF23), a risk factor for premature mortality. To date, clinical implications of iron deficiency and high EPO levels in the general population, and the potential downstream role of FGF23, are unclear. Therefore, we aimed to determine the associations between iron deficiency and higher EPO levels with mortality, and the potential mediating role of FGF23, in a cohort of community-dwelling subjects. Methods and findings We analyzed 6,544 community-dwelling subjects (age 53 ± 12 years; 50% males) who participated in the Prevention of Renal and Vascular End-Stage Disease (PREVEND) study-a prospective population-based cohort study, of which we used the second survey (2001-2003)-and follow-up was performed for a median of 8 years. We measured circulating parameters of iron status, EPO levels, and plasma total FGF23 levels. Our primary outcome was all-cause mortality. In multivariable linear regression analyses, ferritin (ß = -0.43), transferrin saturation (TSAT) (ß = -0.17), hepcidin (ß = -0.36), soluble transferrin receptor (sTfR; ß = 0.33), and EPO (ß = 0.28) were associated with FGF23 level, independent of potential confounders. During median (interquartile range [IQR]) follow-up of 8.2 (7.7-8.8) years, 379 (6%) subjects died. In multivariable Cox regression analyses, lower levels of TSAT (hazard ratio [HR] per 1 standard deviation [SD], 0.84; 95% confidence interval [CI], 0.75-0.95; P = 0.004) and higher levels of sTfR (HR, 1.15; 95% CI 1.03-1.28; P = 0.01), EPO (HR, 1.17; 95% CI 1.05-1.29; P = 0.004), and FGF23 (HR, 1.20; 95% CI 1.10-1.32; P < 0.001) were each significantly associated with an increased risk of death, independent of potential confounders. Adjustment for FGF23 levels markedly attenuated the associations of TSAT (HR, 0.89; 95% CI 0.78-1.01; P = 0.06), sTfR (HR, 1.08; 95% CI 0.96-1.20; P = 0.19), and EPO (HR, 1.10; 95% CI 0.99-1.22; P = 0.08) with mortality. FGF23 remained associated with mortality (HR, 1.15; 95% CI 1.04-1.27; P = 0.008) after adjustment for TSAT, sTfR, and EPO levels. Mediation analysis indicated that FGF23 explained 31% of the association between TSAT and mortality; similarly, FGF23 explained 32% of the association between sTfR and mortality and 48% of the association between EPO and mortality (indirect effect P < 0.05 for all analyses). The main limitations of this study were the observational study design and the absence of data on intact FGF23 (iFGF23), precluding us from discerning whether the current results are attributable to an increase in iFGF23 or in C-terminal FGF23 fragments. Conclusions and relevance In this study, we found that functional iron deficiency and higher EPO levels were each associated with an increased risk of death in the general population. Our findings suggest that FGF23 could be involved in the association between functional iron deficiency and increased EPO levels and death. Investigation of strategies aimed at correcting iron deficiency and reducing FGF23 levels is warranted., Author(s): Michele F. Eisenga 1,*, Maarten A. De Jong 1, Peter Van der Meer 2, David E. Leaf 3, Gerwin Huls 4, Ilja M. Nolte 5, Carlo A. J. M. [...]

Abstract: Basic fibroblast growth factor (bFGF or FGF-2) is widely used to modulate the proliferation and differentiation of certain cell types. An expression and purification system for recombinant human FGF-2 [...]

Fibroblast growth factor 21 (FGF-21), which is a modulator of glucose and lipid homeostasis, acts as a novel therapeutic reagent for many metabolic perturbations. However, its potential as a treatment for cardiovascular disease, especially atherosclerosis (AS) has not been fully explored. Here, we report that recombinant FGF-21 improves resistance to cell damage from oxidative stress in vitro, and from atherosclerosis in vivo. Human umbilical vein endothelial cells (HUVECs) were induced with [H.sub.2][O.sub.2], followed by treatment with high purity recombinant FGF-21. The results indicated that FGF-21 significantly enhanced cell viability and decreased the degree of DNA fragmentation in HUVECs, as caused by [H.sub.2][O.sub.2] stress induction. Further studies revealed that FGF-21 inhibited [H.sub.2][O.sub.2]-induced cell apoptosis by preventing the activation of mitogen-activated protein kinase (MAPK) signaling pathways. In an established rat model, FGF-21 dramatically improved the condition of atherosclerotic rats by decreasing serum levels of total triglyceride (TG), low density lipoprotein cholesterol (LDL-C), and total cholesterol (TC), and by increasing the serum levels of high density lipoprotein cholesterol (HDL-C). FGF-21 also has antioxidant effects in the atherosclerotic rat, such that increased levels of superoxide dismutase, reduced glutathione, and reduced malondialdehyde were observed. These data provide novel insight into the potential use of FGF-21 in the prevention and treatment of human cardiovascular diseases. Key words: FGF-21, HUVECs, oxidative stress, apoptosis. Le facteur de croissance fibroblastique 21 (FGF-21), un modulateur de l'homeostasie du glucose et des lipides, agit comme nouvel agent therapeutique de plusieurs troubles metaboliques. Cependant, son potentiel comme traitement de la maladie cardiovasculaire, notamment l'atherosclerose (AS), n'a pas ete pleinement explore. Les auteurs rapportent ici que le FGF-21 recombinant ameliore la resistance au dommage cellulaire cause par le stress oxydant in vitro et l'atherosclerose in vivo. Des cellules endotheliales de la veine de cordon ombilical humain (HUVEC) ont ete traitees au [H.sub.2][O.sub.2], puis au FGF-21 recombinant de haute purete. Les resultats ont indique que le FGF-21 accroissait significativement la viabilite cellulaire et diminuait le degre de fragmentation d'ADN provoquee chez les cellules HUVEC par le stress du au traitement au [H.sub.2][O.sub.2]. Des etudes additionnelles ont revele que le FGF-21 inhibait l'apoptose induite par le [H.sub.2][O.sub.2] en prevenant l'activation de la signalisation par la voie de MAPK. Dans un modele etabli, le FGF-21 ameliorait de facon importante les conditions des rats atteints d'atherosclerose en diminuant les niveaux seriques des triglycerides totaux (TG), de cholesterol lie aux lipoproteines de faible densite (LDL-C), du cholesterol total (TC) et en augmentant le cholesterol lie aux lipoproteines de haute densite (HDL-C). Le FGF-21 exercait aussi un effet antioxydant chez le rat souffrant d'atherosclerose, car des augmentations de SOD et de GSH et une diminution de MDA ont ete observees. Ces donnees donnent un nouvel apercu du potentiel du FGF-21 dans la prevention et le traitement des maladies cardiovasculaires chez l'humain. [Traduit par la Redaction] Mots-cles: FGF-21, HUVEC, stress oxydant, apoptose., Introduction Atherosclerosis (AS) is a chronic and degenerative disease of the large artery walls. It is the single most important cause of cardiovascular disease (CVD), which is a predominant health [...]

Author(s): Judith Sebestyen VanSickle [sup.1] , Tarak Srivastava [sup.1] , Penny Monachino [sup.1] , Uri S. Alon [sup.1] Author Affiliations: (1) grid.266756.6, 0000 0001 2179 926X, Bone and Mineral Disorders [...]