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Related Concept Videos

Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
The Inner Mitochondrial Membrane01:28

The Inner Mitochondrial Membrane

The inner mitochondrial membrane is the primary site of ATP synthesis. The inner membrane domain that forms a smooth layer adjacent to the outer membrane is called the inner boundary membrane. This domain contains membrane transporters that drive metabolites in and out of the mitochondria.  In contrast, the inner membrane network that invaginates into the matrix space is called the cristae membrane. This domain accounts for principle mitochondrial function as it accommodates the protein...

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Updated: Jun 29, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Mitochondrial dysfunction and HIF1alpha stabilization in inflammation.

Assegid Garedew1, Salvador Moncada

  • 1The Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK.

Journal of Cell Science
|October 2, 2008
PubMed
Summary
This summary is machine-generated.

Activated macrophages develop mitochondrial defects and increased glycolysis, driven by nitric oxide (NO) and HIF1alpha stabilization. This leads to an energy deficit, inhibiting cell proliferation and causing death.

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Area of Science:

  • Cellular metabolism
  • Immunology
  • Mitochondrial function

Background:

  • Macrophages play crucial roles in immune responses.
  • Immune activation can significantly alter cellular energy metabolism.
  • Mitochondrial dysfunction is implicated in various cellular processes.

Purpose of the Study:

  • To investigate the impact of immune activation on macrophage mitochondrial function and energy production.
  • To elucidate the role of nitric oxide (NO) and hypoxia-inducible factor 1-alpha (HIF1alpha) in these metabolic changes.
  • To understand the consequences of metabolic alterations on macrophage proliferation and survival.

Main Methods:

  • Activation of J774.A1 macrophages using interferon gamma and lipopolysaccharide.
  • Measurement of oxygen consumption and ATP generation via oxidative phosphorylation.
  • Assessment of nitric oxide (NO) production and inducible NO synthase activity.
  • Analysis of hypoxia-inducible factor 1-alpha (HIF1alpha) stabilization.
  • Evaluation of glycolytic ATP production and cellular energy balance.

Main Results:

  • Macrophage activation induced mitochondrial defects, inhibiting oxygen consumption and oxidative phosphorylation-dependent ATP generation.
  • Nitric oxide (NO) production by inducible NO synthase was a key factor, consuming oxygen and contributing to mitochondrial dysfunction.
  • A biphasic stabilization of HIF1alpha was observed, with the second phase dependent on NO.
  • Mitochondrial defects and HIF1alpha stabilization synergistically activated glycolysis, increasing ATP production.
  • Despite enhanced glycolysis, the total ATP generated was insufficient for activated cells, leading to an energy deficit.

Conclusions:

  • Immune activation of macrophages leads to significant mitochondrial dysfunction and metabolic reprogramming.
  • Nitric oxide (NO) plays a critical role in mediating these metabolic changes and HIF1alpha stabilization.
  • The resulting energy deficit impairs macrophage proliferation and survival, highlighting the link between metabolism and cell fate.