ArticleJournal of clinical biochemistry and nutrition2011
Mitochondrial disorders in NSAIDs-induced small bowel injury.
Article in Journal of clinical biochemistry and nutrition, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Gut Microbiota in NSAID Enteropathy: Current Evidence and Future Perspectives for Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Targeting SMOX Preserves Optic Nerve Myelin, Axonal Integrity, and Visual Function in Multiple Sclerosis.Biomolecules · 2025Article
- Article
- Actives from the Micro-Immunotherapy Medicine 2LMIREGJournal of inflammation research · 2024Article
- Ketogal Safety Profile in Human Primary Colonic Epithelial Cells and in Mice.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Effect of Weikang Capsule () on Aspirin-Related Gastric and Small Intestinal Mucosal Injury.Chinese journal of integrative medicine · 2021Article
- Current knowledge on non-steroidal anti-inflammatory drug-induced small-bowel damage: a comprehensive review.Journal of gastroenterology · 2020Review
- Prevalence of Gastric and Small-Intestinal Mucosal Injury in Elderly Patients Taking Enteric-Coated Aspirin by Magnetically Controlled Capsule Endoscopy.Gastroenterology research and practice · 2019Article
- Microbiome and intestinal ischemia/reperfusion injury.Journal of clinical biochemistry and nutrition · 2018Review
- Role of non-steroidal anti-inflammatory drugs on intestinal permeability and nonalcoholic fatty liver disease.World journal of gastroenterology · 2017Review
- Ibuprofen Induces Mitochondrial-Mediated Apoptosis Through Proteasomal Dysfunction.Molecular neurobiology · 2016Article
- Colchicine prevents NSAID-induced small intestinal injury by inhibiting activation of the NLRP3 inflammasome.Scientific reports · 2016Article
- Long-term efficacy and safety of rabeprazole in patients taking low-dose aspirin with a history of peptic ulcers: a phase 2/3, randomized, parallel-group, multicenter, extension clinical trial.Journal of clinical biochemistry and nutrition · 2015Article
- Nonsteroidal anti-inflammatory drug-induced visible and invisible small intestinal injury.Journal of clinical biochemistry and nutrition · 2013Article
- Multiple NSAID-induced hits injure the small intestine: underlying mechanisms and novel strategies.Toxicological sciences : an official journal of the Society of Toxicology · 2013Review
- Bisphosphonate-induced gastrointestinal mucosal injury is mediated by mitochondrial superoxide production and lipid peroxidation.Journal of clinical biochemistry and nutrition · 2012Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies using small bowel endoscopy revealed that non-steroidal anti-inflammatory drugs including low-dose aspirin, can often induce small bowel injury. Non-steroidal anti-inflammatory drugs-induced small bowel mucosal injury involves various factors such as enterobacteria, cytokines, and bile. Experimental studies demonstrate that both mitochondrial disorders and inhibition of cyclooxygenases are required for development of non-steroidal anti-inflammatory drugs-induced small bowel injury. Mitochondrion is an organelle playing a central role in energy production in organisms. Many non-steroidal anti-inflammatory drugs directly cause mitochondrial disorders, which are attributable to uncoupling of oxidative phosphorylation induced by opening of the mega channel called mitochondrial permeability transition pore on the mitochondrial membrane by non-steroidal anti-inflammatory drugs. Bile acids and tumor necrosis factor-α also can open the permeability transition pore. The permeability transition pore opening induces the release of cytochrome c from mitochondrial matrix into the cytosol, which triggers a cascade of events that will lead to cell death. Therefore these mitochondrial disorders may cause disturbance of the mucosal barrier function and elevation of the small bowel permeability, and play particularly important roles in early processes of non-steroidal anti-inflammatory drugs-induced small bowel injury. Although no valid means of preventing or treating non-steroidal anti-inflammatory drugs-induced small bowel injury has been established, advances in mitochondrial studies may bring about innovation in the prevention and treatment of this kind of injury.
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