ReviewInternational journal of molecular sciences2019
Polyamine Catabolism in Acute Kidney Injury.
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- AMD1-mediated polyamine metabolism governs tubular repair fate by restraining senescence after kidney injury.Renal failure · 2026Article
- Polyamine metabolism in ischemia reperfusion injury: common mitochondrial mechanisms and organ-specific differences.Journal of translational medicine · 2026Review
- Review
- Key platelet genes play important roles in predicting the prognosis of sepsis.Scientific reports · 2024Article
- Inflammation primes the murine kidney for recovery by activating AZIN1 adenosine-to-inosine editing.The Journal of clinical investigation · 2024Article
- The role of polyamine metabolism in cellular function and physiology.American journal of physiology. Cell physiology · 2024Review
- Polyamine Catabolism and Its Role in Renal Injury and Fibrosis in Mice Subjected to Repeated Low-Dose Cisplatin Treatment.Biomedicines · 2024Article
- Involvement of mammalian SoLute Carriers (SLC) in the traffic of polyamines.Frontiers in molecular biosciences · 2024Review
- Metabolism of Polyamines and Kidney Disease: A Promising Therapeutic Target.Kidney diseases (Basel, Switzerland) · 2023Review
- Inflammation primes the kidney for recovery by activating AZIN1 A-to-I editing.bioRxiv : the preprint server for biology · 2023Article
- Renal, but not platelet or skin, extracellular vesicles decrease oxidative stress, enhance nascent peptide synthesis, and protect from ischemic renal injury.American journal of physiology. Renal physiology · 2023Article
- Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury.Frontiers in cell and developmental biology · 2023Review
- Expression of Polyamine Oxidase in Fibroblasts Induces MMP-1 and Decreases the Integrity of Extracellular Matrix.International journal of molecular sciences · 2022Article
- Spermidine protects against acute kidney injury by modulating macrophage NLRP3 inflammasome activation and mitochondrial respiration in an eIF5A hypusination-related pathway.Molecular medicine (Cambridge, Mass.) · 2022Article
- LncRNA ENSMUST_147219 mediates the progression of ischemic acute kidney injury by targeting the miR-221-5p/IRF6 axis.Apoptosis : an international journal on programmed cell death · 2022Article
- Polyamines and Their Metabolism: From the Maintenance of Physiological Homeostasis to the Mediation of Disease.Medical sciences (Basel, Switzerland) · 2022Review
- Single-cell RNA sequencing in silent corticotroph tumors confirms impaired POMC processing and provides new insights into their invasive behavior.European journal of endocrinology · 2022Article
- Polyamine Metabolism inMedical sciences (Basel, Switzerland) · 2022Review
- Unique Chemistry, Intake, and Metabolism of Polyamines in the Central Nervous System (CNS) and Its Body.Biomolecules · 2022Review
- Metabolic reprogramming in a slowly developing orthologous model of polycystic kidney disease.American journal of physiology. Renal physiology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Acute kidney injury (AKI) refers to an abrupt decrease in kidney function. It affects approximately 7% of all hospitalized patients and almost 35% of intensive care patients. Mortality from acute kidney injury remains high, particularly in critically ill patients, where it can be more than 50%. The primary causes of AKI include ischemia/reperfusion (I/R), sepsis, or nephrotoxicity; however, AKI patients may present with a complicated etiology where many of the aforementioned conditions co-exist. Multiple bio-markers associated with renal damage, as well as metabolic and signal transduction pathways that are involved in the mediation of renal dysfunction have been identified as a result of the examination of models, patient samples, and clinical data of AKI of disparate etiologies. These discoveries have enhanced our ability to diagnose AKIs and to begin to elucidate the mechanisms involved in their pathogenesis. Studies in our laboratory revealed that the expression and activity of spermine/spermidine N
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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.