ArticleBiology2018
Cell Death Patterns Due to Warm Ischemia or Reperfusion in Renal Tubular Epithelial Cells Originating from Human, Mouse, or the Native Hibernator Hamster.
Article in Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Cross-talk among novel programmed cell death pathways: a decisive network in renal ischemia-reperfusion injury.Frontiers in immunology · 2026Review
- Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury.The Journal of clinical investigation · 2025Review
- In renal proximal tubular epithelial cells of the hibernator Syrian hamster, anoxia-reoxygenation-induced reactive oxygen species bursts do not trigger a DNA damage response and cellular senescence.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2025Article
- Evaluation of urine glutathione peroxidase 4 in cats with chronic kidney disease.Frontiers in veterinary science · 2025Article
- Deeper insight into ferroptosis: association with Alzheimer's, Parkinson's disease, and brain tumors and their possible treatment by nanomaterials induced ferroptosis.Redox report : communications in free radical research · 2023Review
- Emerging significance and therapeutic targets of ferroptosis: a potential avenue for human kidney diseases.Cell death & disease · 2023Review
- Vitamin A and retinoid signaling in the kidneys.Pharmacology & therapeutics · 2023Review
- Routes of Albumin Overload Toxicity in Renal Tubular Epithelial Cells.International journal of molecular sciences · 2023Article
- Inhibition of Malate Dehydrogenase-2 Protects Renal Tubular Epithelial Cells from Anoxia-Reoxygenation-Induced Death or Senescence.Biomolecules · 2022Article
- Indoleamine 2,3 Dioxygenase 1-The Potential Link between the Innate Immunity and the Ischemia-Reperfusion-Induced Acute Kidney Injury?International journal of molecular sciences · 2022Review
- Ferroptosis induces membrane blebbing in placental trophoblasts.Journal of cell science · 2022Article
- CCN2 Aggravates the Immediate Oxidative Stress-DNA Damage Response following Renal Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2021Article
- The Role of Indoleamine 2,3-Dioxygenase in Renal Tubular Epithelial Cells Senescence under Anoxia or Reoxygenation.Biomolecules · 2021Article
- Role of indoleamine 2,3-dioxygenase in ischemia-reperfusion injury of renal tubular epithelial cells.Molecular medicine reports · 2021Article
- Farnesoid X receptor promotes renal ischaemia-reperfusion injury by inducing tubular epithelial cell apoptosis.Cell proliferation · 2021Article
- A Role for Human Renal Tubular Epithelial Cells in Direct Allo-Recognition by CD4+ T-Cells and the Effect of Ischemia-Reperfusion.International journal of molecular sciences · 2021Article
- Reoxygenation induces reactive oxygen species production and ferroptosis in renal tubular epithelial cells by activating aryl hydrocarbon receptor.Molecular medicine reports · 2021Article
- Autophagy Dynamics and Modulation in a Rat Model of Renal Ischemia-Reperfusion Injury.International journal of molecular sciences · 2020Article
- Mistimed HBiomedical reports · 2020Article
- Ferroptosis and kidney diseases.International urology and nephrology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemia⁻reperfusion injury contributes to the pathogenesis of many diseases, with acute kidney injury included. Hibernating mammals survive prolonged bouts of deep torpor with a dramatic drop in blood pressure, heart, and breathing rates, interspersed with short periods of arousal and, consequently, ischemia⁻reperfusion injury. Clarifying the differences under warm anoxia or reoxygenation between human cells and cells from a native hibernator may reveal interventions for rendering human cells resistant to ischemia⁻reperfusion injury. Human and hamster renal proximal tubular epithelial cells (RPTECs) were cultured under warm anoxia or reoxygenation. Mouse RPTECs were used as a phylogenetic control for hamster cells. Cell death was assessed by both cell imaging and lactate dehydrogenase (LDH) release assay, apoptosis by cleaved caspase-3, autophagy by microtubule-associated protein 1-light chain 3 B II (LC3B-II) to LC3B-I ratio, necroptosis by phosphorylated mixed-lineage kinase domain-like pseudokinase, reactive oxygen species (ROS) fluorometrically, and lipid peroxidation, the end-point of ferroptosis, by malondialdehyde. Human cells died after short periods of warm anoxia or reoxygenation, whereas hamster cells were extremely resistant. In human cells, apoptosis contributed to cell death under both anoxia and reoxygenation. Although under reoxygenation, ROS increased in both human and hamster RPTECs, lipid peroxidation-induced cell death was detected only in human cells. Autophagy was observed only in human cells under both conditions. Necroptosis was not detected in any of the evaluated cells. Clarifying the ways that are responsible for hamster RPTECs escaping from apoptosis and lipid peroxidation-induced cell death may reveal interventions for preventing ischemia⁻reperfusion-induced acute kidney injury in humans.
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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.