Correction: Sleep and Biological Rhythms (2025) 24:259–266 10.1007/s41105-025-00625-5
In this article, Fig. 2 was duplicated as Figs. 3 and 4 but should have appeared as shown in this correction.
Fig. 3 Effect of HIF-1a/BNIP3 pathway on ATP, MMP, and mitochondrial morphology in IH-induced HK-2 cells. A, B Mitochondrial dysfunction under IH: IH exposure reduced ATP production and MMP in HK-2 cells; HIF-1a/BNIP3 knockdown amplified these deficits; BNIP3 overexpression rescued mitochondrial parametres during HIF-1a inhibition. C Increased autophagosomes (blue arrow) /autophagolysosomes (red arrow) in IH vs normoxia. HIF-1a/BNIP3 knockdown suppressed autophagic structure formation; Combined HIF-1a inhibition and BNIP3 overexpression restored autophagy. A Cellular ATP concentration detected with ATP assay kit. B MMP level detected with JC-1. C Mitochondrial ultrastructure under TEM. Autophagosome (blue arrow) and autophagolysosome (red arrow) were observed
Fig. 4 Effect of HIF-1α/BNIP3 pathway on LC3B immunofluorescence colocalization in IH-induced HK-2 cells. Confocal microscopy revealed elevated LC3B (autophagosomes) and COX IV (mitochondrial) fluorescence density in IH-exposed compared to normoxia control; siHIF-1α/siBNIP3 suppressed fluorescence intensity under IH conditions. BNIP3 overexpression counteracted the suppression caused by HIF-1α knockdown. Left: Representative images under a confocal microscope. LC3B (green) and COX IV (red) were used to treat cells to mark autophagosomes and mitochondria. The overlap zone of LC3B and COX IV was defined as immunofluorescence colocalization. Right: Bar charts of colocalization coefficient of LC3B and COX IV
The original article has been corrected.
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