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Related Concept Videos

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Hypoxia01:23

Hypoxia

Hypoxia is a medical condition characterized by an inadequate oxygen supply to body tissues. It typically manifests as a bluish discoloration of the skin and mucosae, especially in fair-skinned individuals, when hemoglobin (Hb) saturation drops below 75%.
Types of Hypoxia
There are four primary types of hypoxia, each resulting from a different cause:
1. Anemic hypoxia: This type occurs due to insufficient oxygen delivery caused by a lack of red blood cells (RBCs) or RBCs with abnormal or...

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Related Experiment Video

Updated: Jun 23, 2026

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
06:23

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

PFKFB3 Mediated Glycolytic Reprogramming Drives Vascular Endothelial Injury Under Chronic Intermittent Hypoxia.

Shi Qi Li1,2, Yi Wang1,2, Liu Zhang1,2

  • 1Department of Respiratory and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

International Journal of Biological Sciences
|June 22, 2026
PubMed
Summary
This summary is machine-generated.

Obstructive sleep apnea (OSA) causes endothelial inflammation via chronic intermittent hypoxia (CIH). Our study reveals PFKFB3, a glycolytic enzyme, drives this inflammation through a HIF-1α-PFKFB3-H3K18la feedback loop, offering new therapeutic targets for cardiovascular disease.

Keywords:
PFKFB3chronic intermittent hypoxiaendothelial inflammationglycolysisobstructive sleep apnea

Related Experiment Videos

Last Updated: Jun 23, 2026

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
06:23

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

Area of Science:

  • Cardiovascular Biology
  • Metabolic Regulation
  • Sleep Medicine

Background:

  • Metabolic and inflammatory pathways are central to cardiovascular disease.
  • Obstructive sleep apnea (OSA), marked by chronic intermittent hypoxia (CIH), is a significant cardiovascular risk factor.
  • Endothelial inflammation from CIH is key, but its metabolic drivers are unclear.

Purpose of the Study:

  • To investigate the role of phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) in endothelial inflammation induced by CIH.
  • To elucidate the molecular mechanisms linking CIH, metabolic changes, and endothelial dysfunction.
  • To identify potential therapeutic targets for OSA-related cardiovascular pathology.

Main Methods:

  • Examined PFKFB3 expression in endothelial cells (ECs) under CIH.
  • Assessed glycolysis, mitochondrial respiration, and inflammatory markers.
  • Utilized endothelial-specific PFKFB3 knockout models and pharmacological inhibition.
  • Investigated the hypoxia-inducible factor 1α (HIF-1α)/PFKFB3 pathway and H3K18 lactylation (H3K18la).

Main Results:

  • CIH upregulated PFKFB3 in ECs, increasing glycolysis and inflammation while suppressing mitochondrial respiration.
  • PFKFB3 deficiency or inhibition normalized glycolysis and reduced endothelial injury.
  • CIH induced HIF-1α, which upregulates PFKFB3, creating a positive feedback loop with lactate and H3K18la.
  • Targeting the HIF-1α/PFKFB3 axis ameliorated EC inflammatory and glycolytic profiles.

Conclusions:

  • PFKFB3 is a critical metabolic mediator of endothelial inflammation in CIH.
  • A novel HIF-1α-PFKFB3-H3K18la feedback loop drives OSA-associated endothelial dysfunction.
  • This pathway represents a potential therapeutic target for cardiovascular complications of OSA.