ArticleEuropean journal of trauma and emergency surgery : official publication of the European Trauma Society2022
Remote ischemic postconditioning protects against crush-induced acute kidney injury via down-regulation of apoptosis and senescence.
Article in European journal of trauma and emergency surgery : official publication of the European Trauma Society, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Ferroptosis in acute kidney injury following crush syndrome: A novel target for treatment.Journal of advanced research · 2023Pooled it
- Pre-earthquake kidney function is a predictor of outcomes in earthquake-related crush syndrome.BMC nephrology · 2025Article
- The role of ferroptosis in acute kidney injury: mechanisms and potential therapeutic targets.Molecular and cellular biochemistry · 2025Review
- Combined effect of intermittent hemostasis and a modified external hemorrhage control device in a lethal swine model.Heliyon · 2024Article
- The Evaluation of Different Treatment Approaches in Patients With Earthquake-Related Crush Syndrome.Cureus · 2023Article
- Clinical and Epidemiological Characteristics of Rhabdomyolysis: A Retrospective Study.International journal of clinical practice · 2023Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAcute renal failure due to crush syndrome is one of the leading causes of death in disasters. Ischemic Postconditioning (IPC) is a potentially effective strategy to protect against ischemic reperfusion injury, but a few studies noted its protective effect in crush induced acute kidney injury (AKI). Hence, this study investigated the optimal IPC strategy to prevent crush induced AKI and reveal related cellular mechanisms.
methodsThe right lower extremities of rabbits were constantly compressed for 8 h and then performed five cycles of clamping and releasing the femoral artery and vein before depression using a clip. In terms of the duration of clamping and releasing, the animals were randomly divided into 5 groups, Control, IPC-5sec, IPC-30sec, IPC-1min, and IPC-5min groups; 6 rabbits for each group. Biomarkers of inflammation, renal function, renal tubular injury, and muscular injury, apoptosis, and cellular senescence in kidney were detected.
resultsSix hours after decompression, the levels of Serum Creatine (SCr), Blood Urea Nitrogen (BUN), K+, and Interleukin-6 (IL-6) in IPC-1min and IPC-5min groups were lower than Control, with a statistically significant difference. The morphological study of Periodic Acid-Schiff (PAS) staining demonstrated that 6 h after decompression, IPC-1min can attenuate renal tubular damage renal tubule. Meanwhile, the level of Neutrophil Gelatinase-Associated Lipocalin (NGAL) in circulation in the IPC-30sec, IPC-1min, and IPC-5min groups was significantly decreased compared with the Control group, 2 h after decompression. On the other hand, the levels of serum Creatine Kinase (CK) and Myoglobin (Mb), and the morphological change of muscular damage detected by hematoxylin and eosin (H&E) staining in IPC-1min-treated group were significantly lower than Control group 6 hours after decompression. Further results of the cellular mechanism showed that the apoptotic markers of Terminal deoxynucleotidyl Transferase-mediated dUTP Nick End Labeling (TUNEL) and Caspase3 and the cell senescent markers of senescence-associated β-galactosidase (SA-β-Gal) and nuclear LAMNB1 have changed significantly in the IPC-1min group, compared with the control group.
conclusionsPerforming 5 cycles of 1-min IPC would be a convenient, time-saving, and effective method to prevent crush-induced AKI by attenuating the release of nephrotoxic substances after decompression and downregulation of the expression of apoptosis and cellular senescence biomarkers.
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