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Related Concept Videos

Inflammation01:38

Inflammation

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Overview
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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%.
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After glycolysis, the charged pyruvate molecules enter the mitochondria via active transport and undergo three enzymatic reactions. These reactions ensure that pyruvate can enter the next metabolic pathway so that energy stored in the pyruvate molecules can be harnessed by the cells.
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Salt stress—which can be triggered by high salt concentrations in a plant’s environment—can significantly affect plant growth and crop production by influencing photosynthesis and the absorption of water and nutrients.
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Related Experiment Video

Updated: Feb 12, 2026

Glutamate and Hypoxia as a Stress Model for the Isolated Perfused Vertebrate Retina
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Glutamate and Hypoxia as a Stress Model for the Isolated Perfused Vertebrate Retina

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Hypoxia, oxidative stress and inflammation.

Trudy McGarry1, Monika Biniecka2, Douglas J Veale2

  • 1The Department of Molecular Rheumatology, Trinity College Dublin, Ireland.

Free Radical Biology & Medicine
|March 31, 2018
PubMed
Summary
This summary is machine-generated.

Inflammatory arthritis causes joint damage due to poor oxygen supply and cellular metabolic shifts. Understanding these changes in the hypoxic microenvironment is key to developing new treatments.

Keywords:
Altered cellular metabolismDysregulated angiogenesisHypoxiaInflammatory arthritisMitochondrial dysfunctionOxidative stress

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Area of Science:

  • Immunology
  • Cell Biology
  • Pathophysiology

Background:

  • Inflammatory arthritis involves synovial proliferation and leukocyte infiltration, leading to joint destruction.
  • Synovial microvasculature dysfunction impairs oxygen supply, creating a hypoxic environment.
  • Hypoxia, mitochondrial dysfunction, and oxidative stress drive disease pathogenesis.

Purpose of the Study:

  • To elucidate the metabolic adaptations of synovial cells in inflammatory arthritis.
  • To understand the role of hypoxia-induced signaling in disease progression.
  • To investigate the interplay between oxidative stress and mitochondrial function.

Main Methods:

  • Analysis of cellular metabolism in synovial tissue.
  • Investigation of hypoxia-induced signaling pathways.
  • Assessment of mitochondrial function and oxidative stress markers.

Main Results:

  • Synovial cells switch to a highly active metabolic state to support proliferation.
  • Metabolic intermediates accumulate, acting as signaling molecules.
  • This metabolic shift exacerbates inflammation and oxidative damage.

Conclusions:

  • Cellular metabolic reprogramming is a critical component of inflammatory arthritis pathogenesis.
  • Targeting metabolic pathways may offer novel therapeutic strategies.
  • Further research into hypoxia-driven inflammation is warranted.