Key result
LCN2 showed high sensitivity and specificity in discriminating children with idiopathic short stature from those with growth hormone deficiency, precocious puberty, and normal controls.
Why the study?
Idiopathic short stature pathology remains unclear, with no effective diagnostic markers or therapeutic strategies currently available.
Observational (n=348)
LCN2 is identified as a novel diagnostic biomarker and potential therapeutic target for idiopathic short stature, with experimental evidence showing it impairs bone growth.
Answers are grounded in this paper and cite their sources.
LCN2 merits exploration as ISS biomarker and target; leaves open clinical translation pending human studies.
Idiopathic short stature (ISS) is the most common paediatric endocrine disease. However, the underlying pathology of ISS remains unclear. Currently, there are no effective diagnostic markers or therapeutic strategies available for ISS. In this study, we aimed to identify differential plasma protein expression and novel biomarkers in patients with ISS, and elucidate the biological functions of candidate proteins in ISS pathogenesis. Four specimen pairs from four ISS children and age-/sex-matched control individuals were subjected to proteomics analysis, and 340 samples of children with a mean age 9.73 ± 0.24 years were utilized to further verify the differentially expressed proteins by enzyme-linked immunosorbent assay (ELISA). The receiver-operating characteristic (ROC) curve and the area under the ROC curve (AUC) were plotted. A total of 2040 proteins were identified, of which 84 were differentially expressed. In vitro and in vivo experiments confirmed the biological functions of these candidate proteins. LCN2 overexpression in ISS was verified using ELISA. Meanwhile, LCN2 showed high sensitivity and specificity in discriminating children with ISS from those with growth hormone deficiency, precocious puberty and normal control individuals. The upregulated expression of LCN2 not only suppressed food intake but also impaired chondrocyte proliferation and bone growth in chondrocytes and rats. As a result, the rats presented a short-stature phenotype. Subsequently, we found that bone growth inhibition recovered after LCN2 overexpression was stopped in immature rats. To our knowledge, this is the first study to report that LCN2 may be a significant target for ISS diagnosis and treatment.
No takes yet. Share an insight, caveat, or question.
Liu et al. (2022) conducted an observational in Idiopathic short stature (n=348). Elevated LCN2 expression vs. Normal controls, growth hormone deficiency, and precocious puberty was evaluated on Differential plasma protein expression and diagnostic accuracy (AUC). LCN2 showed high sensitivity and specificity in discriminating children with idiopathic short stature from those with growth hormone deficiency, precocious puberty, and normal controls.
Synapse has enriched 10 related papers. Consider them for comparative context: