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Related Concept Videos

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...
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,...
Cellular Injury IV: Necrosis01:16

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,...
The Electron Transport Chain01:30

The Electron Transport Chain

The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q in...

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Related Experiment Video

Updated: Jun 12, 2026

A Preclinical Model of Sepsis-Induced Myopathy with Disuse in Mice
04:01

A Preclinical Model of Sepsis-Induced Myopathy with Disuse in Mice

Published on: June 14, 2024

Mitochondrial dysfunction during sepsis.

Luciano Cesar Pontes Azevedo1

  • 1Hospital Sirio-Libanes - Research and Education Institute, Rua Cel Nicolau dos Santos 69, Bela Vista, São Paulo, Brazil. luciano.azevedo@hsl.org.br

Endocrine, Metabolic & Immune Disorders Drug Targets
|June 1, 2010
PubMed
Summary

Sepsis-induced organ failure may be an adaptive response, not just damage. Restoring mitochondrial function could be key to patient recovery and survival in intensive care.

Area of Science:

  • Critical care medicine
  • Mitochondrial biology
  • Pathophysiology of sepsis

Background:

  • Sepsis and multiple organ failure are leading causes of death in intensive care units.
  • Mitochondria play a critical role in the pathophysiology of sepsis and organ dysfunction.
  • Mitochondrial dysfunction severity correlates with patient outcomes.

Purpose of the Study:

  • To review the role of mitochondria in sepsis-induced organ failure.
  • To explore mechanisms of mitochondrial dysfunction in sepsis.
  • To discuss therapeutic strategies targeting mitochondrial recovery.

Main Methods:

  • Review of current literature on sepsis, organ failure, and mitochondrial function.
  • Analysis of mechanisms including reactive oxygen species, hypoxia, hormonal influences, and protein expression.

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  • Examination of adaptive state hypotheses and recovery processes.
  • Main Results:

    • Mitochondrial dysfunction is a key factor in sepsis-related organ failure.
    • Mechanisms involve direct damage, enzyme inhibition, and altered gene expression.
    • Organ failure may be an adaptive "hibernation" state, not solely cell death.
    • Recovery of mitochondrial function precedes clinical improvement.

    Conclusions:

    • Mitochondrial dysfunction is central to sepsis and organ failure.
    • Organ failure might be a protective adaptive response.
    • Therapeutic strategies aimed at stimulating mitochondrial biogenesis offer promise for improving patient outcomes.