ArticlePloS one2015
TLR9 Mediates Remote Liver Injury following Severe Renal Ischemia Reperfusion.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
18 citing papers in PubMed, 37 citations in OpenAlex.
- The journey of boswellic acids from synthesis to pharmacological activities.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Thiostrepton-Nanomedicine, a TLR9 Inhibitor, Attenuates Sepsis-Induced Inflammation in Mice.Mediators of inflammation · 2023Article
- Toll-like receptor 9 deficiency induces osteoclastic bone loss via gut microbiota-associated systemic chronic inflammation.Bone research · 2022Article
- Expanding role of deoxyribonucleic acid-sensing mechanism in the development of lifestyle-related diseases.Frontiers in cardiovascular medicine · 2022Review
- Treprostinil alleviates hepatic mitochondrial injury during rat renal ischemia-reperfusion injury.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Article
- Mitochondrial DNA-Mediated Inflammation in Acute Kidney Injury and Chronic Kidney Disease.Oxidative medicine and cellular longevity · 2021Review
- Use of TLR9 and TLR7/8 agonists in combination with d-galactosamine in exploring models for distinct severities of systemic inflammation relative to liver injury.Physiological research · 2020Article
- Review
- TLR9 in MAFLD and NASH: At the Intersection of Inflammation and Metabolism.Frontiers in endocrinology · 2020Review
- Metabolic Flexibility and Innate Immunity in Renal Ischemia Reperfusion Injury: The Fine Balance Between Adaptive Repair and Tissue Degeneration.Frontiers in immunology · 2020Review
- TLR9 and COVID-19: A Multidisciplinary Theory of a Multifaceted Therapeutic Target.Frontiers in pharmacology · 2020Article
- Mechanisms and therapeutic targets of ischemic acute kidney injury.Kidney research and clinical practice · 2019Review
- Gut derived-endotoxin contributes to inflammation in severe ischemic acute kidney injury.BMC nephrology · 2019Article
- Mitochondrial DNA Is a Pro-Inflammatory Damage-Associated Molecular Pattern Released During Active IBD.Inflammatory bowel diseases · 2018Article
- Kidney Proximal Tubular TLR9 Exacerbates Ischemic Acute Kidney Injury.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Released Mitochondrial DNA Following Intestinal Ischemia Reperfusion Induces the Inflammatory Response and Gut Barrier Dysfunction.Scientific reports · 2018Article
- Advances in the understanding of mitochondrial DNA as a pathogenic factor in inflammatory diseases.F1000Research · 2017Review
- Sex Differences in the Effect of Resveratrol on DSS-Induced Colitis in Mice.Gastroenterology research and practice · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemia reperfusion injury is a common cause of acute kidney injury and is characterized by tubular damage. Mitochondrial DNA is released upon severe tissue injury and can act as a damage-associated molecular pattern via the innate immune receptor TLR9. Here, we investigated the role of TLR9 in the context of moderate or severe renal ischemia reperfusion injury using wild-type C57BL/6 mice or TLR9KO mice. Moderate renal ischemia induced renal dysfunction but did not decrease animal well-being and was not regulated by TLR9. In contrast, severe renal ischemia decreased animal well-being and survival in wild-type mice after respectively one or five days of reperfusion. TLR9 deficiency improved animal well-being and survival. TLR9 deficiency did not reduce renal inflammation or tubular necrosis. Rather, severe renal ischemia induced hepatic injury as seen by increased plasma ALAT and ASAT levels and focal hepatic necrosis which was prevented by TLR9 deficiency and correlated with reduced circulating mitochondrial DNA levels and plasma LDH. We conclude that TLR9 does not mediate renal dysfunction following either moderate or severe renal ischemia. In contrast, our data indicates that TLR9 is an important mediator of hepatic injury secondary to ischemic acute kidney injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.