Growth differentiation factor 15 (GDF15), a member of the transforming growth factor-beta superfamily, is expressed in several human organs. In particular, it is highly expressed in the placenta, prostate, and liver. The expression of GDF15 increases under cellular stress and pathological conditions. Although numerous transcription factors directly up-regulate the expression of GDF15, the receptors and downstream mediators of GDF15 signal transduction in most tissues have not yet been determined. Glial cell-derived neurotrophic factor family receptor α-like protein was recently identified as a specific receptor that plays a mediating role in anorexia. However, the specific receptors of GDF15 in other tissues and organs remain unclear. As a marker of cell stress, GDF15 appears to exert different effects under different pathological conditions. Cell senescence may be an important pathogenetic process and could be used to assess the progression of various lung diseases, including COVID-19. As a key member of the senescence-associated secretory phenotype protein repertoire, GDF15 seems to be associated with mitochondrial dysfunction, although the specific molecular mechanism linking GDF15 expression with ageing remains to be elucidated. Here, we focus on research progress linking GDF15 expression with the pathogenesis of various chronic lung diseases, including neonatal bronchopulmonary dysplasia, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and pulmonary hypertension, suggesting that GDF15 may be a key biomarker for diagnosis and prognosis. Thus, in this review, we aimed to provide new insights into the molecular biological mechanism and emerging clinical data associated with GDF15 in lung-related diseases, while highlighting promising research and clinical prospects.
Partial deletion of 10p chromosome is a rare chromosomal aberration. Submicroscopic deletion of 10p15.3 is mainly related to cognitive deficits, speech disorders, motor delay, and hypotonia with the deleted region ranging from 0.15 to 4 Mb. The clinical phenotype is mainly determined by the ZMYND11 and DIP2C genes. Here, we report a rare case of feeding difficulties, hypocalcemia, and psychomotor retardation. Our patient has a 12.48 Mb deletion in 10p15.3–10p13, which is the second case of large 10p deletion among reported cases thus far.
Purpose: To evaluate the diagnostic effect of umbilical cord blood procalcitonin (PCT) on fetal inflammatory response syndrome (FIRS). Methods: This prospective study assessed preterm infants (100 with FIRS and 124 controls) with gestational age <32 weeks. The groups were compared in terms of the incidence of complications associated with preterm birth. To identify whether FIRS was an independent risk factor for complications of preterm birth, odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by multivariable logistic regression models. Finally, we clarified the diagnostic efficiency by receiver operating characteristic curves. Results: Univariate analysis showed that the incidence of natural delivery, premature rupture of membranes (PROM) > 18h, antenatal antibiotic usage, chorioamnionitis, umbilical cord blood PCT, gestational age (GA), small for gestational age (SGA), bronchopulmonary dysplasia (BPD), early-onset sepsis (EOS), necrotizing enterocolitis (NEC), white matter injury (WMI), retinopathy of prematurity (ROP), and mortality were higher in the case group than the control group (p < 0.05). Multivariable analysis confirmed a significant association between FIRS and complications of preterm birth. The level of umbilical cord blood PCT of preterm infants could be used as a noninvasive diagnostic index for FIRS (cut-off value: 0.276 ng/ml). Conclusions: Umbilical cord blood PCT may be a reliable noninvasive diagnostic biomarker for FIRS. Chorioamnionitis, natural delivery, and the level of umbilical cord blood PCT are independent risk factors for FIRS in preterm infants, while GA was a protective factor for FIRS. FIRS is an independent risk factor for BPD, EOS, NEC, WMI and ROP.
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