The impact of MicroRNAs on Irritable Bowel Syndrome: A Systematic Review
Irritable Bowel Syndrome (IBS) is characterized by changes in bowel habits such as changes in consistency and increased fecal frequency, flatulence, tenesmus and abdominal pain. The condition progresses with periods of remission, in which symptoms reduce or disappear for weeks, months or even years. In another spectrum, relapses may occur with an increase in the frequency and intensity of signs and symptoms. Despite affecting individuals at any stage of life, approximately 5% to 10% of the world's healthy population, the underlying causes and exact mechanisms that lead to the development of IBS are not yet fully understood. Recently, advances have revealed that several non-protein-coding and highly evolutionarily conserved miRNAs (20–24 nucleotides) are intimately involved in the pathogenesis of Irritable Bowel Syndrome (IBS). MiRNAs play a fundamental role in the post-transcriptional regulation of gene expression through mechanisms that depend on specific sequences, binding to messenger RNAs (mRNAs) and modulating translation and consequent protein synthesis. In the context of Irritable Bowel Syndrome (IBS), miRNA-29a, miRNA-125b, miRNA-16 and miRNA-144 increase the permeability of the intestinal barrier, allowing the entry of unwanted substances into the bloodstream, which contributes to the symptoms of IBS. IBS. Other miRNAs, such as miRNA-15/107, miRNA-24, miRNA-29, miRNA-199, miRNA-200 and miRNA-495, play a crucial role in regulating hyperalgesia responses. Inflammatory responses, in turn, are mainly controlled by miRNA-181 and miRNA-510, which record patients' signs and symptoms. Currently, available medications are mainly aimed at relieving symptoms, without addressing the etiology of the disease. Therefore, understanding epigenetics is essential to develop therapeutic approaches that can act not only during periods of remission and relapses, but also with the curative objective of the syndrome.
The impact of MicroRNAs on Irritable Bowel Syndrome: A Systematic Review
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DOI: https://doi.org/10.22533/at.ed.1594662404079
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Palavras-chave: MicroRNAs; Irritable Bowel Syndrome (IBS); Inflammation; Molecular mechanisms
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Keywords: MicroRNAs; Irritable Bowel Syndrome (IBS); Inflammation; Molecular mechanisms
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Abstract:
Irritable Bowel Syndrome (IBS) is characterized by changes in bowel habits such as changes in consistency and increased fecal frequency, flatulence, tenesmus and abdominal pain. The condition progresses with periods of remission, in which symptoms reduce or disappear for weeks, months or even years. In another spectrum, relapses may occur with an increase in the frequency and intensity of signs and symptoms. Despite affecting individuals at any stage of life, approximately 5% to 10% of the world's healthy population, the underlying causes and exact mechanisms that lead to the development of IBS are not yet fully understood. Recently, advances have revealed that several non-protein-coding and highly evolutionarily conserved miRNAs (20–24 nucleotides) are intimately involved in the pathogenesis of Irritable Bowel Syndrome (IBS). MiRNAs play a fundamental role in the post-transcriptional regulation of gene expression through mechanisms that depend on specific sequences, binding to messenger RNAs (mRNAs) and modulating translation and consequent protein synthesis. In the context of Irritable Bowel Syndrome (IBS), miRNA-29a, miRNA-125b, miRNA-16 and miRNA-144 increase the permeability of the intestinal barrier, allowing the entry of unwanted substances into the bloodstream, which contributes to the symptoms of IBS. IBS. Other miRNAs, such as miRNA-15/107, miRNA-24, miRNA-29, miRNA-199, miRNA-200 and miRNA-495, play a crucial role in regulating hyperalgesia responses. Inflammatory responses, in turn, are mainly controlled by miRNA-181 and miRNA-510, which record patients' signs and symptoms. Currently, available medications are mainly aimed at relieving symptoms, without addressing the etiology of the disease. Therefore, understanding epigenetics is essential to develop therapeutic approaches that can act not only during periods of remission and relapses, but also with the curative objective of the syndrome.
- Laura Garcia
- Gustavo Leone Caroni
- Lucas Maitan Francisco Alves
- Nara Manella
- Maria Eduarda Scaramal Scolari
- Mylla Ortega Brandão
- Gustavo Oldani Batista Cozza
- Yaskara Harumi Kato
- Júlia Maschio da Silva
- Anna Julia Prata de Campos
- Luís Henrique Lima Negro Júnior
- Alcielle Alves de Oliveira