Back to Search
Start Over
[Research advances in the mechanism of Toll-like receptor 4 mediated intestinal injury and inflammatory response in necrotizing enterocolitis].
- Source :
-
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology [Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi] 2025 Jan; Vol. 41 (1), pp. 57-63. - Publication Year :
- 2025
-
Abstract
- Necrotizing enterocolitis (NEC) is an intestinal inflammatory and necrotic disease seen in premature infants, and remains the leading cause of death resulted from gastrointestinal diseases in premature infants. The specific pathogenesis of NEC is still unclear. In recent years, a lot of studies have reported that Toll-like receptor 4 (TLR4) plays a key role in the pathogenesis of NEC. TLR4, which is abundantly expressed in intestinal epithelial cells of premature infants, binds to bacterial lipopolysaccharide (LPS) to activate downstream signaling pathways, leading to disruption of intestinal epithelial integrity and bacterial translocation, resulting in intestinal ischemic necrosis and inflammatory responses, which may rapidly progress to severe sepsis, multiple organ dysfunction, and death. This paper reviews the mechanism of TLR4-related signaling pathways in intestinal epithelial injury and inflammatory responses in newborns with NEC, providing a reference to study new therapeutic targets for NEC.
- Subjects :
- Humans
Infant, Newborn
Inflammation metabolism
Animals
Intestinal Mucosa metabolism
Intestines pathology
Intestines immunology
Infant, Premature
Enterocolitis, Necrotizing metabolism
Enterocolitis, Necrotizing etiology
Enterocolitis, Necrotizing immunology
Enterocolitis, Necrotizing pathology
Toll-Like Receptor 4 metabolism
Toll-Like Receptor 4 physiology
Signal Transduction
Subjects
Details
- Language :
- Chinese
- ISSN :
- 1007-8738
- Volume :
- 41
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology
- Publication Type :
- Academic Journal
- Accession number :
- 39799426