ArticleInternational journal of experimental pathology2023
Interaction between mitochondrial homeostasis and barrier function in lipopolysaccharide-induced endothelial cell injury.
Article in International journal of experimental pathology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Gut microbiota-dependent mechanisms and efficacy of natural polysaccharides in multitarget antidepressant therapy: a systematic review.Frontiers in psychiatry · 2026Pooled it
- Alterations of endothelial cell bioenergetics in congenital diaphragmatic hernia.Pediatric research · 2026Article
- Exploring Endotoxemia in Age-Related Macular Degeneration, Glaucoma, and Diabetic Retinopathy.Investigative ophthalmology & visual science · 2026Review
- hucMSCs alleviate LPS-induced endothelial glycocalyx damage by secreting Cxcl12 to activate CXCR4.Stem cell research & therapy · 2026Article
- Article
- Identification of mitochondria-related biomarkers for acute respiratory distress syndrome.Scientific reports · 2025Article
- Preoperative TNF-α predicts uneventful postoperative outcomes in patients undergoing colorectal cancer surgery.Scientific reports · 2025Observational
- Establishment of an Apical-Out Organoid Model for Directly Assessing the Function of Postbiotics.Journal of microbiology and biotechnology · 2024Article
- The Role of Endothelial Cell Mitophagy in Age-Related Cardiovascular Diseases.Aging and disease · 2024Review
- Interaction between mitochondrial homeostasis and barrier function in lipopolysaccharide-induced endothelial cell injury.International journal of experimental pathology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
This study aimed to investigate the effects of mitochondrial homeostasis on lipopolysaccharide (LPS)-induced endothelial cell barrier function and the mechanisms that underlie these effects. Cells were treated with LPS or oligomycin (mitochondrial adenosine triphosphate synthase inhibitor) and the mitochondrial morphology, mitochondrial reactive oxygen species (mtROS), and mitochondrial membrane potential (ΔΨm) were evaluated. Moreover, the shedding of glycocalyx-heparan sulphate (HS), the levels of HS-specific degrading enzyme heparanase (HPA), and the expression of occludin and zonula occludens (ZO-1) of Tight Junctions (TJ)s, which are mediated by myosin light chain phosphorylation (p-MLC), were assessed. Examining the changes in mitochondrial homeostasis showed that adding heparinase III, which is an exogenous HPA, can destroy the integrity of glycocalyx. LPS simultaneously increased mitochondrial swelling, mtROS, and ΔΨm. Without oligomycin effects, HS, HPA levels, and p-MLC were found to be elevated, and the destruction of occludin and ZO-1 increased. Heparinase III not only damaged the glycocalyx by increasing HS shedding but also increased mitochondrial swelling and mtROS and decreased ΔΨm. Mitochondrial homeostasis is involved in LPS-induced endothelial cell barrier dysfunction by aggravating HPA and p-MLC levels. In turn, the integrated glycocalyx protects mitochondrial homeostasis.
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Registered trials
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