Related Experiment Video

Updated: Jun 14, 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 function and dysfunction in sepsis

Martina Wendel1, Axel R Heller

  • 1Fachklinik Prinzregent Luitpold, Scheidegg, Germany. MartinaWendel@gmx.de

Wiener Medizinische Wochenschrift (1946)
|April 6, 2010
PubMed

Insights

Pathogen responses can damage mitochondria via oxidative stress, depleting cellular energy (NAD+). Novel therapies targeting this response protected mitochondrial function and improved organ function in studies.

Area of Science:

  • Mitochondrial biology
  • Cellular pathophysiology
  • Immunology

Background:

  • Mitochondria generate cellular ATP, but their function is compromised during pathogen responses.
  • Peroxynitrite, a reactive compound, inhibits mitochondrial enzymes and damages cellular components.
  • Oxidative stress activates PARP, depleting NAD+ and promoting inflammation.

Purpose of the Study:

  • To investigate the impact of pathogen-induced pathophysiologic processes on mitochondrial function.
  • To explore therapeutic strategies for mitigating mitochondrial damage and preserving cellular respiration.

Main Methods:

  • Experimental studies investigating host response to pathogens.
  • Assessment of mitochondrial enzyme activity and cellular respiration.
  • Evaluation of novel therapeutic interventions targeting oxidative stress and signaling pathways.

Main Results:

  • Peroxynitrite formation inhibits mitochondrial enzymes and causes cellular damage.
  • NAD+ depletion due to PARP activation impairs respiratory chain function and exacerbates inflammation.
  • Therapeutic strategies ameliorated host response, protected mitochondrial function, and preserved cellular respiration.

Conclusions:

  • Mitochondrial dysfunction is a critical consequence of the host's response to pathogens.
  • Targeting oxidative stress and related signaling pathways offers a promising therapeutic approach.
  • Preserving mitochondrial function is crucial for maintaining organ function during infection.

More Related Videos

Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue08:56

Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue

Published on: May 17, 2018

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,...
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...
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,...
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,...
ATP Synthase: Mechanism01:48

ATP Synthase: Mechanism

In animals, the mitochondrial F1F0 ATP synthase is the key protein that synthesizes ATP molecules through a complex catalytic mechanism. While the nuclear genome encodes the majority of ATP synthase subunits, the mitochondrial genome encodes some of the enzyme's most critical components. The formation of this multi-subunit enzyme is a complex multi-step process regulated at the level of transcription, translation, and assembly. Defects in one or more of these steps can result in decreased ATP...