ArticleSleep and biological rhythms2026
Mitophagy protects renal tubular epithelial cells from intermittent hypoxia-induced injury via the HIF-1α/BNIP3 pathway.
Article in Sleep and biological rhythms, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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
- Erratum issued
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to investigate the role of mitophagy mediated by the hypoxia-inducible factor-1α (HIF-1α)/Bcl-2/adenovirus E1B 19-kDa interacting protein (BNIP3) pathway in mitigating renal injury induced by intermittent hypoxia (IH), a hallmark of obstructive sleep apnea (OSA). Human renal tubular epithelial cells (RTECs) were exposed to IH conditions using a hypoxia-reoxygenation chamber for 24 h. Cells were divided into five groups: normoxia, IH, IH with HIF-1α siRNA (IH + si-HIF-1α), IH with BNIP3 siRNA (IH + siBNIP3), and IH with HIF-1α siRNA plus BNIP3 overexpression (IH + si-HIF-1α + BNIP3). Cell viability, apoptosis, mitochondrial morphology, and mitophagy levels were assessed using flow cytometry, western blotting, transmission electron microscopy, and immunofluorescence. Under IH conditions, inhibition of HIF-1α or BNIP3 significantly reduced cell viability, increased apoptosis, disrupted mitochondrial structure, and decreased mitophagy levels in RTECs. Overexpression of BNIP3 in the presence of HIF-1α inhibition restored mitophagy levels, attenuated cellular damage and apoptosis, and improved mitochondrial morphology. These findings demonstrate that mitophagy mediated by the HIF-1α/BNIP3 signaling pathway plays a protective role in IH-induced renal injury, suggesting that targeted enhancement of mitophagy may provide a potential therapeutic strategy for OSA-related kidney dysfunction. Supplementary Information: The online version contains supplementary material available at 10.1007/s41105-025-00625-5.
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.