Abstract
Although more than 1 in 4 men develop symptomatic inguinal hernia during their lifetime, the molecular mechanism behind inguinal hernia remains unknown. Here, we explored the protein-protein interaction network built on known inguinal hernia-causative genes to identify essential and common downstream proteins for inguinal hernia formation. We discovered that PIK3R1, PTPN11, TGFBR1, CDC42, SOS1, and KRAS were the most essential inguinal hernia-causative proteins and UBC, GRB2, CTNNB1, HSP90AA1, CBL, PLCG1, and CRK were listed as the most commonly-involved downstream proteins. In addition, the transmembrane receptor protein tyrosine kinase signaling pathway was the most frequently found inguinal hernia-related pathway. Our in silico approach was able to uncover a novel molecular mechanism underlying inguinal hernia formation by identifying inguinal hernia-related essential proteins and potential common downstream proteins of inguinal hernia-causative proteins.
Highlights
IntroductionInguinal hernia repair is one of the most routine operations worldwide
In general surgery, inguinal hernia repair is one of the most routine operations worldwide
Our results show that PIK3R1, PTPN11, TGFBR1, CDC42, and SOS1 are probably the most essential proteins involved in human hernia formation
Summary
Inguinal hernia repair is one of the most routine operations worldwide. More than one in four men can expect to undergo inguinal hernia repair during their lifetime [1, 2]. Inguinal hernias can cause severe complications, such as incarceration and strangulation and currently, surgery is the only treatment option for the management of inguinal hernia. Complications such as postoperative pain, nerve injury, infection, and recurrence continue to challenge surgeons and patients [5, 7,8,9]. Despite its prevalence in patients, the molecular mechanisms that predispose individuals to develop inguinal hernias are still unknown
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