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Published on: October 12, 2017
Vesicoureteral reflux and the extracellular matrix connection
Fatima Tokhmafshan1, Patrick D Brophy2, Rasheed A Gbadegesin3,4
1Department of Human Genetics, McGill University, Montreal, QC, Canada.
Primary vesicoureteral reflux (VUR) in children may stem from defects in the extracellular matrix (ECM) at the ureterovesical junction. This review examines the role of smooth muscle, ECM, and related gene mutations in VUR development.
Area of Science:
- Pediatric Urology
- Developmental Biology
- Connective Tissue Biology
Background:
- Primary vesicoureteral reflux (VUR) is a common congenital condition affecting the urinary tract.
- VUR is characterized by the abnormal backward flow of urine from the bladder to the ureters.
- A developmental defect in the ureterovesical junction is the primary cause of VUR.
Purpose of the Study:
- To review the function of smooth muscle and its extracellular matrix (ECM) microenvironment in the ureterovesical junction concerning VUR.
- To explore the potential association between VUR and mutations in genes encoding ECM components.
- To understand the developmental basis of VUR by examining the structural integrity of the ureterovesical junction.
Main Methods:
- Literature review focusing on the pathophysiology of VUR.
- Analysis of the role of extracellular matrix (ECM) and smooth muscle in ureterovesical junction function.
- Examination of genetic studies linking ECM-related genes to VUR.
Main Results:
- The ureterovesical junction's anti-reflux mechanism relies on the proper function of ureter and bladder wall musculature.
- Defects in the extracellular matrix (ECM) are hypothesized to contribute to the developmental abnormalities leading to VUR.
- A higher prevalence of VUR in individuals with connective tissue disorders suggests a link to ECM dysfunction.
Conclusions:
- The extracellular matrix (ECM) and smooth muscle of the ureterovesical junction are critical for preventing vesicoureteral reflux (VUR).
- Genetic defects affecting ECM components may underlie the etiology of primary VUR.
- Further research into ECM-related genes could reveal novel insights into VUR pathogenesis and potential therapeutic targets.
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