ReviewInternational urology and nephrology2026
Mitophagy in kidney transplantation ischemia-reperfusion injury.
Review in International urology and nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Redox control at the ER-mitochondria interface in kidney transplantation: MAM-centered stress signaling and translational organoid platforms.Redox biology · 2026Review
- The Current Application Prospects of Nanomedicine in Renal Ischemia-Reperfusion Injury.International journal of nanomedicine · 2026Review
- PANoptosis nexus in ischemia-reperfusion injury: from integrated cell death mechanisms to novel therapeutic opportunities.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Renal ischemia-reperfusion injury (IRI) remains a major challenge impacting graft survival following transplantation. During the ischemic phase, mitochondrial dysfunction leads to adenosine triphosphate (ATP) depletion and calcium overload. Upon reperfusion, reactive oxygen species (ROS) are generated, exacerbating mitochondrial damage and triggering inflammatory responses. This process is associated not only with delayed graft function (DGF) but also with allograft dysfunction. Mitochondria, serving as the high-energy-demand hub of the kidney, require precise regulation of their dynamic balance and mitophagy. Mitophagy selectively removes damaged mitochondria to maintain cellular homeostasis. In the context of IRI, mitophagy exhibits a bidirectional regulatory role: moderate activation can improve energy metabolism, whereas excessive or insufficient activation may exacerbate renal injury. To provide new insights for enhancing graft survival rates, this paper examines the molecular mechanisms, therapeutic targets, and dual regulatory roles involved.
Indexed as
Identifiers
40890535What 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.