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Related Concept Videos

Mitochondria01:37

Mitochondria

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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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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.
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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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The Electron Transport Chain

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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.
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Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q...
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Techniques to Induce and Quantify Cellular Senescence
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Senolytic and senomorphic interventions to defy senescence-associated mitochondrial dysfunction.

Jan O Nehlin1

  • 1Department of Clinical Research, Copenhagen University Hospital, Amager and Hvidovre, Hvidovre, Denmark.

Advances in Protein Chemistry and Structural Biology
|July 12, 2023
PubMed
Summary

Cellular senescence, marked by mitochondrial dysfunction, drives aging pathologies. Senotherapeutics targeting these senescent cells can improve healthspan by enhancing mitochondrial function and reducing aging burdens.

Keywords:
AgingGerosuppressorsMitochondriaSenescenceSenolyticsSenomorphicsSenotherapeutics

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Area of Science:

  • Gerontology
  • Cellular Biology
  • Mitochondrial Medicine

Background:

  • Cellular senescence accumulation contributes to age-associated diseases, frailty, and mortality.
  • Mitochondrial dysfunction is a key factor triggering cellular senescence and contributing to organismal aging.
  • Senescent cells, characterized by their senescence burden, impact overall healthspan.

Purpose of the Study:

  • To outline the mechanisms of senotherapeutics targeting mitochondria.
  • To explore senotherapeutics that address senescence-associated mitochondrial dysfunction.
  • To investigate combining geroprotective interventions with senotherapeutics for enhanced mitochondrial health.

Main Methods:

  • Review of senotherapeutics including senolytics, senomorphics, senostatics, and gerosuppressors.
  • Analysis of cellular models for inducing senescence via mitochondrial dysfunction.
  • Examination of senotherapeutic mechanisms targeting mitochondria and senescence.

Main Results:

  • Senotherapeutics can eliminate senescent cells (senolytics) or modulate their secretome (senomorphics/senostatics).
  • Mitochondrial dysfunction is a direct trigger for specific types of cellular senescence.
  • Targeting mitochondria in senescent cells offers a therapeutic avenue for aging.

Conclusions:

  • Senotherapeutics offer promising strategies to combat age-associated pathologies by targeting senescent cells.
  • Enhancing mitochondrial energy metabolism, biogenesis, and turnover is crucial for extending healthspan.
  • Combining geroprotective interventions with senotherapeutics can mitigate aging by improving mitochondrial health and function.