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Related Concept Videos

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...
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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,...
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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,...
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Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...

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Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue
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Published on: May 17, 2018

Mitochondrial function in sepsis.

Victor Jeger1, Siamak Djafarzadeh, Stephan M Jakob

  • 1Department of Intensive Care Medicine, University Hospital Inselspital and University of Bern, Bern, Switzerland.

European Journal of Clinical Investigation
|March 19, 2013
PubMed
Summary
This summary is machine-generated.

Mitochondrial dysfunction in sepsis is highly variable and not consistently proven as the cause of multiple organ failure. Further research is needed, especially in older patients with comorbidities.

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Published on: February 8, 2017

Area of Science:

  • Critical Care Medicine
  • Mitochondrial Biology
  • Sepsis Pathophysiology

Background:

  • The role of mitochondrial dysfunction in sepsis-induced multiple organ dysfunction and failure remains debated.
  • This review critically examines existing evidence on mitochondrial function during sepsis.

Purpose of the Study:

  • To evaluate the evidence for impaired mitochondrial function in the context of sepsis.
  • To synthesize findings from experimental animal models and clinical studies.

Main Methods:

  • Focused review of original studies on mitochondrial function in experimental sepsis (rodents, pigs) and human sepsis.
  • Exclusion of in vitro studies on isolated cells/tissues.
  • Literature search of PubMed from 1964 to July 2012.

Main Results:

  • No consistent pattern of sepsis-related mitochondrial dysfunction was observed across species.
  • High variability in mitochondrial function was noted, even in control conditions and across different organs.
  • Discrepancies in findings may stem from diverse sepsis models, experimental durations, and measurement techniques.

Conclusions:

  • Mitochondrial function in sepsis is highly variable, organ-specific, and dynamic.
  • Current data, primarily from young, healthy animals, do not support mitochondrial dysfunction as a universal cause of multiple organ failure in sepsis.
  • Future studies should investigate mitochondrial function in older patients and those with comorbidities.