ArticleBioengineering & translational medicine2026
Kidney organoids as a novel platform to evaluate heat-stress-induced acute kidney injury pathogenesis.
Article in Bioengineering & translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Kidney organoids as a novel platform to evaluate heat-stress-induced acute kidney injury pathogenesis.Bioengineering & translational medicine · 2026Article
- Energy metabolic dysregulation in heat stroke: from mitochondrial dysfunction to multi-organ failure mechanisms and targeted intervention.Frontiers in pharmacology · 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
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is a serious condition with significant global impact. To explore mechanisms and biomarkers of heat-stress-induced AKI, we used human kidney organoids derived from induced pluripotent stem cells via suspension culture. Organoids were exposed to 37, 39, and 41°C. At 41°C, we found the viability decreased over time, with cytoskeleton damage, impaired tubule absorption, apoptosis, and collagen deposition. Under extreme heat (41°C), elevated AKI markers KIM-1 and NGAL, along with cell cycle arrest markers TIMP-2*IGFBP7 were detected. Notably, TIMP-2*IGFBP7 appeared at 12 h post-exposure, preceding NGAL and KIM-1. Nascent and steady-state RNA analyses revealed suppressed oxidative phosphorylation and ATP metabolism, along with elevated histone expression, implicating their roles in heat-induced AKI. The data support that kidney organoids serve as a valuable model for investigating heat-induced AKI, providing insights into early injury biomarkers that are valuable for the development of treatments.
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.