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Genetic factors contributing to the development of inguinal hernias

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Summary

This on-demand teaching session, led by Datis Kalali from the University of Cyprus Medical School, explores the intricate genetic factors contributing to the development of inguinal hernias. Often considered a multifactorial disease, this session delves into the possible genetic influences on inguinal hernias, specifically focusing on genes linked to altered risk of herniation. The session will provide a comprehensive overview of associated genes, including collagen genes, elastin gene, matrix metalloproteinase genes, and other gene families influential in embryonic development and muscle formation. An important factor for general and visceral surgery, this session will equip medical professionals with insights from genome-wide association studies and encourage further research in diverse ethnic populations. Perfect for those keen on understanding the molecular mechanisms behind common surgical issues -- be prepared to uncover the genetic secrets of inguinal hernias.

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Learning objectives

  1. Understand the role of extracellular matrix in the development of inguinal hernias.
  2. Comprehend the function of different genes, such as the collagen genes, the elastin gene, the Wilms tumor protein gene, etc., in inguinal herniation.
  3. Evaluate the contributions of genetic factors to the development of inguinal hernias.
  4. Analyze the results of genome-wide association studies exploring susceptible genetic loci associated with inguinal herniation.
  5. Recognize the need for further research, in different ethnic populations, to provide better insights into the genetic factors contributing to the development of inguinal hernias.
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Genetic factors contributing to the development of inguinal hernias Datis Kalali University of Cyprus, Medical School Abstract Molecular mechanisms of inguinal herniation in the field of general and visceral surgery and can be viewed asders multifactorial diseases. Although the molecular mechanism that led to predistortion to inguinal herniation still remain unclear, is well knownfetal fetal development and mechanisms contributing to weaker muscles ofcts. the abdominal wall can greatly increase the ri▪ Extracellular Matrix (ECM) is critical. performed in all major electronic databases using keywords and Boolean operators to retrieve all available literature related to theType III collagen topic. Due to the narrative nature of the reviewresult weaker structure. Genetic factors, undoubtedly, can interfere wi▪ Elastin fibers are reduced in hernia and therefore play major role in developing hernias. To this end, the present narrative review provides an overview of genes with altered herniation. Moreover, the results of genome-wide association studiested; T enascin-X (GWAS) exploring susceptible genetic loci assocideficiency increases risk studies and GWAS need to be conducted in different ethnicontrol populations so as to provide better insights. Genes in inguinal herniation Introduction ▪ Collagen genes ▪ Inguinal hernias are a common ▪ The elastin gene surgical issue of organs (usually intestines) herniating through the ▪ Matrix metalloproteinase genes abdominal wall. ▪ The Wilms tumor protein gene (codes for a transcription factor, responsible • Prevalence: 9% in men, 1% in women. for the development of the urogenital • Types: Direct (through abdominal system). ▪ The EGF-containing fibulin-like wall), Indirect (through inguinal ring). extracellular matrix protein-1 gene • Surgery is the only treatment; (encodes for protein regulating the composition of the extracellular matrix) recurrence is possible. • Genetic predisposition is gaining ▪ The T-box transcription factor genes attention. (encode for a family of proteins vital for embryonic development) Genetic factors contributing to the development ▪ The lysyl oxidase like-1 gene of inguinal hernias (encodes for an enzyme necessary for the biosynthesis of elastin). ▪ Sirtuin genes (encode for a total of 7 proteins, that contribute to muscle formation and differentiation).