ArticlePediatric surgery international2020
Lysosomal overloading and necrotizing enterocolitis.
Article in Pediatric surgery international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- [Silybin inhibits fibrosis after glaucoma filtration surgery in rabbits by promoting fibroblast autophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Antenatal Ureaplasma infection induces ovine small intestinal goblet cell defects: a strong link with NEC pathology.Tissue barriers · 2023Article
- A CRISPR screen in intestinal epithelial cells identifies novel factors for polarity and apical transport.eLife · 2023Article
- Remote ischemic conditioning causes CD4 T cells shift towards reduced cell-mediated inflammation.Pediatric surgery international · 2022Article
- Knockdown of FAM225B inhibits the progression of the hypertrophic scar following glaucoma surgery by inhibiting autophagy.Molecular medicine reports · 2021Article
- Prenatal Immunity and Influences on Necrotizing Enterocolitis and Associated Neonatal Disorders.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
purposeIntestinal absorption in premature infants occurs via direct epithelial cellular endocytosis and degradation by intracellular lysosomes. Autophagy is a mechanism by which cytoplasmic organelles contribute to lysosomal degradation. However, excessive autophagy can lead to cell death. The purpose of this study was to investigate whether autophagy and endocytosis are present in the small intestinal mucosa during experimental necrotizing enterocolitis (NEC).
methodsNEC was induced by gavage feeding of hyperosmolar formula, lipopolysaccharide and hypoxia between P5 and P9 (ethical approval 44032). Breastfed mice were used as control. Distal ileum was harvested on P5, P7 and P9 and analyzed for intestinal epithelial cellular morphology as well as autophagy/lysosomal activity, and cell death. Groups were compared using Student's t test.
resultsDuring NEC, giant lysosomes were present in the intestinal villi, with some exceeding their degradation ability leading to their rupture. The NEC group had significantly increased inflammation and autophagy activity, decreased lysosome activity, and increased apoptosis compared to control.
conclusionsNEC induction causes excessive autophagy and endocytosis leading to lysosomal overloading, lysosomal membrane permeabilization and rupture which results in cell death. These novel findings may help to clarify the pathogenesis of NEC. Reduction of lysosome overload and assisting in their degradation capability may reduce the burden of NEC.
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