The significance of Pax2 expression in the ureter epithelium of children with vesicoureteric reflux

Zheng, Yibing; Xu, Jing; Guo, Wei; Xu, Hong; Chen, Jing; Shen, Qian; Zhang, Xin; Zhai, Yi­hui

doi:10.1016/j.humpath.2015.01.007

Cited by 5 publications

(2 citation statements)

References 37 publications

(38 reference statements)

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“…Moreover, accumulating evidence demonstrated that miR-497 bind with PAX2 and elevated cell apoptosis (Lin et al, 2016). High PAX2 expression was found to be related with cell apoptosis (Zheng et al, 2015). Like the previous studies, in this study, we demonstrated that miR-362-3p enhanced cell apoptosis, evidenced by elevation of cleaved-caspase-3, cleaved-PARP and Bax protein levels, as well as reduction of Bcl-2 protein level in SCI rats.…”

Section: Discussionsupporting

confidence: 79%

MicroRNA-362-3p attenuates motor deficit following spinal cord injury via targeting paired box gene 2

Liu

Zhang

et al. 2019

J. Integr. Neurosci.

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Section: Discussionsupporting

confidence: 79%

MicroRNA-362-3p attenuates motor deficit following spinal cord injury via targeting paired box gene 2

Liu

Zhang

et al. 2019

J. Integr. Neurosci.

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“…Furthermore, PAX2 was identified as a shared gene between RS and dilating VUR. Mutations in the PAX2 gene have previously been implicated in kidney abnormalities, including VUR [53][54][55]. The hepatocyte nuclear factor 1β (HNF1β), associated with kidney pathology in CAKUT patients, was detected in the RS group [56][57][58].…”

Section: Discussionmentioning

confidence: 99%

Genetic determinants of renal scarring in children with febrile UTI

Rosenblad,

Lindén,

Ambite

et al. 2024

Pediatr Nephrol

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Background Febrile urinary tract infections (UTIs) are among the most severe bacterial infections in infants, in which a subset of patients develops complications. Identifying infants at risk of recurrent infections or kidney damage based on clinical signs is challenging. Previous observations suggest that genetic factors influence UTI outcomes and could serve as predictors of disease severity. In this study, we conducted a nationwide survey of infant genotypes to develop a strategy for infection management based on individual genetic risk. Our aims were to identify genetic susceptibility variants for renal scarring (RS) and genetic host factors predisposing to dilating vesicoureteral reflux (VUR) and recurrent UTIs. Methods To assess genetic susceptibility, we collected and analyzed DNA from blood using exome genotyping. Disease-associated genetic variants were identified through bioinformatics analysis, including allelic frequency tests and odds ratio calculations. Kidney involvement was defined using dimercaptosuccinic acid (DMSA) scintigraphy. Results In this investigation, a cohort comprising 1087 infants presenting with their first episode of febrile UTI was included. Among this cohort, a subset of 137 infants who underwent DMSA scanning was subjected to gene association analysis. Remarkable genetic distinctions were observed between patients with RS and those exhibiting resolved kidney involvement. Notably, the genetic signature indicative of renal scarring prominently featured mitochondrial genes. Conclusions In this nationwide study of genetic susceptibility to RS after febrile UTIs in infancy, we identified a profile dominated by mitochondrial polymorphisms. This profile can serve as a predictor of future complications, including RS and recurrent UTIs. Graphical abstract

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