ArticleInternational journal of molecular sciences2022
Mild Therapeutic Hypothermia Protects from Acute and Chronic Renal Ischemia-Reperfusion Injury in Mice by Mitigated Mitochondrial Dysfunction and Modulation of Local and Systemic Inflammation.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Artificial hibernation: A new technique for protecting neural tissue and organs.Neural regeneration research · 2026Article
- Mild Hypothermia Alleviates Ischemia and Reperfusion Injury by Activating PINK1/Parkin Mitophagy.Neurochemical research · 2026Article
- Interplay between ischemia-reperfusion and metabolic reprogramming.Apoptosis : an international journal on programmed cell death · 2026Review
- Contrast-enhanced ultrasound and photoacoustic imaging to assess early and late renal ischemia-reperfusion injuries in male mice.Physiological reports · 2026Article
- The interaction between ferroptosis and myocardial ischemia-reperfusion injury: molecular mechanisms and potential therapeutic targets.European journal of medical research · 2025Review
- Perioperative multivariate analysis and risk prediction of acute kidney injury after cardiac surgery: Based on dynamic temperature changes during cardiopulmonary bypass.Journal of anesthesia and translational medicine · 2025Article
- Mitochondria dysfunction, a potential cytoprotection target against ischemia-reperfusion injury in a mouse stroke model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Cold-Inducible RNA-Binding Protein in Cardiac Arrest and Renal Ischemia-Reperfusion Injury: A Translational Approach.JACC. Basic to translational science · 2025Article
- Investigation into the influence of mild hypothermia on regulating ferroptosis through the P53-SLC7A11/GPX4 signaling pathway in sepsis-induced acute lung injury.Intensive care medicine experimental · 2025Article
- Mild therapeutic hypothermic protection activates the PI3K/AKT signaling pathway to inhibit TRPM7 and suppress ferroptosis induced by myocardial ischemia‑reperfusion injury.Molecular medicine reports · 2024Article
- The future of artificial hibernation medicine: protection of nerves and organs after spinal cord injury.Neural regeneration research · 2024Review
- Heat Shock Protein 70 Is Involved in the Efficiency of Preconditioning with Cyclosporine A in Renal Ischemia Reperfusion Injury by Modulating Mitochondrial Functions.International journal of molecular sciences · 2023Article
- The effects of mild hypothermia on the electrode insertion trauma in a murine whole organ cochlea culture.Frontiers in neuroscience · 2023Article
- Clinical study of renal artery cold perfusion combined with laparoscopic nephron retention in the treatment of complex renal angiomyolipoma.Frontiers in oncology · 2023Article
- New Strategies Protecting from Ischemia/Reperfusion.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Renal ischemia-reperfusion (IR) injury can lead to acute kidney injury, increasing the risk of developing chronic kidney disease. We hypothesized that mild therapeutic hypothermia (mTH), 34 °C, applied during ischemia could protect the function and structure of kidneys against IR injuries in mice. In vivo bilateral renal IR led to an increase in plasma urea and acute tubular necrosis at 24 h prevented by mTH. One month after unilateral IR, kidney atrophy and fibrosis were reduced by mTH. Evaluation of mitochondrial function showed that mTH protected against IR-mediated mitochondrial dysfunction at 24 h, by preserving CRC and OX-PHOS. mTH completely abrogated the IR increase of plasmatic IL-6 and IL-10 at 24 h. Acute tissue inflammation was decreased by mTH (IL-6 and IL1-β) in as little as 2 h. Concomitantly, mTH increased TNF-α expression at 24 h. One month after IR, mTH increased TNF-α mRNA expression, and it decreased TGF-β mRNA expression. We showed that mTH alleviates renal dysfunction and damage through a preservation of mitochondrial function and a modulated systemic and local inflammatory response at the acute phase (2-24 h). The protective effect of mTH is maintained in the long term (1 month), as it diminished renal atrophy and fibrosis, and mitigated chronic renal inflammation.
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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.