ArticleBioscience reports2022
The role of nitric oxide in sepsis-associated kidney injury.
Article in Bioscience reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Research hotspots and future trends in sepsis-associated acute kidney injury: a bibliometric and visualization analysis.Frontiers in medicine · 2024Pooled it
- Mechanistic Insights Into Acute Kidney Injury Complicating Invasive Pulmonary Aspergillosis in Adults.Cureus · 2026Review
- Analysis of PANoptosis-related genes in septic cardiomyopathy by bioinformatics, machine learning and experimental validation.Experimental and therapeutic medicine · 2026Article
- Impact of Melatonin on Sepsis-Associated Acute Kidney Injury in Rat Model of Lipopolysaccharide Endotoxemia.Current issues in molecular biology · 2026Article
- Oxidative stress and endoplasmic reticulum stress in acute kidney injury: mechanistic crosstalk and therapeutic modulation.Frontiers in medicine · 2026Review
- The relationship between estimated pulse wave velocity and 28-day mortality in patients with sA-AKI: a retrospective cohort analysis of the MIMIC-IV database.Renal failure · 2025Article
- Investigating the Role of Empagliflozin in the Pathological Progress of Ischemia-Reperfusion Injury in Rat Kidneys: The Involvement of Nitric Oxide.Advanced pharmaceutical bulletin · 2025Article
- ATPflugers Archiv : European journal of physiology · 2025Article
- Kim-1-targeted multimodal nanoprobes for early diagnosis and monitoring of sepsis-induced acute kidney injury.Apoptosis : an international journal on programmed cell death · 2025Article
- Role of AT1angiotensin receptor antagonist in pulmonary complications induced by renal ischemia-reperfusion injury in male and female rats.BMC nephrology · 2025Article
- Functionalized extracellular vesicles of mesenchymal stem cells for regenerative medicine.Journal of nanobiotechnology · 2025Review
- TAK-242 improves sepsis-associated acute kidney injury in rats by inhibiting the TLR4/NF-κB signaling pathway.Renal failure · 2024Article
- Investigating the efficacy of dapsone in treating sepsis induced by cecal ligation and puncture surgery in male mice.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Review
- The renoprotective effect of Tibolone in sepsis-induced acute kidney injury.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2024Article
- The role of Chinese herbal medicine in the regulation of oxidative stress in treating hypertension: from therapeutics to mechanisms.Chinese medicine · 2024Review
- The roles of G protein-coupled receptor kinase 2 in renal diseases.Journal of cellular and molecular medicine · 2024Review
- Review
- Acute Kidney Injury in Sepsis.International journal of molecular sciences · 2024Review
- Oxidative stress and the role of redox signalling in chronic kidney disease.Nature reviews. Nephrology · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is one of the leading causes of acute kidney injury (AKI), and several mechanisms including microcirculatory alterations, oxidative stress, and endothelial cell dysfunction are involved. Nitric oxide (NO) is one of the common elements to all these mechanisms. Although all three nitric oxide synthase (NOS) isoforms are constitutively expressed within the kidneys, they contribute in different ways to nitrergic signaling. While the endothelial (eNOS) and neuronal (nNOS) isoforms are likely to be the main sources of NO under basal conditions and participate in the regulation of renal hemodynamics, the inducible isoform (iNOS) is dramatically increased in conditions such as sepsis. The overexpression of iNOS in the renal cortex causes a shunting of blood to this region, with consequent medullary ischemia in sepsis. Differences in the vascular reactivity among different vascular beds may also help to explain renal failure in this condition. While most of the vessels present vasoplegia and do not respond to vasoconstrictors, renal microcirculation behaves differently from nonrenal vascular beds, displaying similar constrictor responses in control and septic conditions. The selective inhibition of iNOS, without affecting other isoforms, has been described as the ideal scenario. However, iNOS is also constitutively expressed in the kidneys and the NO produced by this isoform is important for immune defense. In this sense, instead of a direct iNOS inhibition, targeting the NO effectors such as guanylate cyclase, potassium channels, peroxynitrite, and S-nitrosothiols, may be a more interesting approach in sepsis-AKI and further investigation is warranted.
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Registered trials
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