ArticleJCI insight2022
Remote ischemic preconditioning causes transient cell cycle arrest and renal protection by a NF-κB-dependent Sema5B pathway.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- NFKB1 as a key player in Tumor biology: from mechanisms to therapeutic implications.Cell biology and toxicology · 2025Pooled it
- Impact of propofol or sevoflurane on the renoprotective effect of remote ischaemic preconditioning in cardiac surgery: the HypnoRenalRIP randomised clinical trial.British journal of anaesthesia · 2025Trial
- Review
- Circulating miRNAs Correlate With rIPC-Induced Cardioprotection and Its Impairment in Diabetic Myocardial Infarction via AMPK Signalling.Journal of cellular and molecular medicine · 2026Article
- The interplay between type 2 diabetes mellitus and sepsis: a scoping review.International journal of medical sciences · 2026Article
- Biomarker-driven risk stratification and early intervention in acute kidney injury: a comprehensive review from early warning to clinical response.Frontiers in medicine · 2026Review
- Systemic downregulation of EV-associated MiRNAs following remote ischemic preconditioning.Scientific reports · 2025Article
- Article
- Remote Ischemic Preconditioning Attenuates Mitochondrial Dysfunction and Ferroptosis of Tubular Epithelial Cells by Inhibiting NOX4-ROS Signaling in Acute Kidney Injury.International journal of biological sciences · 2025Article
- Article
- Research hotspots and frontiers of preconditioning in cerebral ischemia: A bibliometric analysis.Heliyon · 2024Review
- Renoprotective effects of remote ischemic preconditioning on acute kidney injury induced by repeated tourniquet application in patients undergoing extremity surgery.Frontiers in medicine · 2024Article
- Cellular senescence and kidney aging.Clinical science (London, England : 1979) · 2023Review
- Effects of remote ischemic preconditioning on renal protection in patients undergoing robot-assisted laparoscopic partial nephrectomy.Journal of robotic surgery · 2023Article
- NephroCheck at 10: addressing unmet needs in AKI diagnosis and risk stratification.Clinical kidney journal · 2023Article
- Targeting HMGB1: A Potential Therapeutic Strategy for Chronic Kidney Disease.International journal of biological sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury increases morbidity and mortality, and previous studies have shown that remote ischemic preconditioning (RIPC) reduces the risk of acute kidney injury after cardiac surgery. RIPC increases urinary high mobility group box protein-1 (HMGB1) levels in patients, and this correlates with kidney protection. Here, we show that RIPC reduces renal ischemia-reperfusion injury and improves kidney function in mice. Mechanistically, RIPC increases HMGB1 levels in the plasma and urine, and HMGB1 binds to TLR4 on renal tubular epithelial cells, inducing transcriptomic modulation of renal tubular epithelial cells and providing renal protection, whereas TLR4 activation on nonrenal cells was shown to contribute to renal injury. This protection is mediated by activation of induction of AMPKα and NF-κB; this induction contributes to the upregulation of Sema5b, which triggers a transient, protective G1 cell cycle arrest. In cardiac surgery patients at high risk for postoperative acute kidney injury, increased HMGB1 and Sema5b levels after RIPC were associated with renal protection after surgery. The results may help to develop future clinical treatment options for acute kidney injury.
Indexed as
Identifiers
What OpenQuestion holds
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.