ArticleFrontiers in cell and developmental biology2026
Integrated toxicogenomic and single-nucleus transcriptomic analyses prioritize SDHB and NDUFAB1 in mitochondrial respiration-associated remodeling during cisplatin-induced acute kidney injury.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
No grant is acknowledged in the PubMed record.
Abstract
Background: Cisplatin-induced acute kidney injury (Cis-AKI) is a multifactorial nephrotoxic syndrome involving proximal tubular injury, oxidative and inflammatory stress, mitochondrial dysfunction, metabolic disturbance, and regulated cell death. However, the molecular targets linking cisplatin-associated toxicogenomic changes to AKI remain incompletely characterized. Methods: We integrated network toxicology, transcriptomic analysis, single-nucleus RNA sequencing, and Results: A total of 214 shared genes were identified between the cisplatin-associated and AKI-related gene sets. These genes were mainly enriched in cellular respiration, electron transport, oxidoreductase activity, respiratory-chain complexes, and oxidative phosphorylation. Network analysis prioritized SDHB and NDUFAB1 within the respiration-associated gene network. In the cisplatin-induced mouse AKI dataset, Aco2, Aco1, Sdhb, and Aldh2 were significantly upregulated under stringent criteria, whereas additional respiration- and metabolism-related genes, including Ndufab1, met a secondary differential expression threshold. Human single-nucleus analysis revealed distinct cell-type-specific expression patterns of SDHB and NDUFAB1, with increased SDHB and decreased NDUFAB1 expression in proximal tubular cells. Pseudotime analysis showed a more pronounced late-stage increase in SDHB, whereas NDUFAB1 displayed weaker dynamics. In cisplatin-treated BUMPT cells, Havcr1 and Lcn2 were increased, Bcl2 was decreased, and Casp3 was increased. Among the selected candidate genes, Sdhb, Aco2, Aldh2, Ndufs2, and Uqcrc1 were upregulated, whereas Ndufab1 showed a modest decrease. NicheNet analysis further suggested that TGFB1-related signaling may contribute to proximal tubular transcriptional remodeling. Conclusion: This study prioritizes SDHB and NDUFAB1 within a respiration-associated gene network in Cis-AKI and demonstrates that they exhibit distinct expression patterns during proximal tubular injury. These findings highlight respiration-associated remodeling and proximal tubular state transition in cisplatin-induced 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.