Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

13.6K
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,...
13.6K
Mitochondrial Membranes01:45

Mitochondrial Membranes

17.5K
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,...
17.5K
The Inner Mitochondrial Membrane01:28

The Inner Mitochondrial Membrane

4.9K
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...
4.9K
Mitochondria01:37

Mitochondria

21.1K
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,...
21.1K
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

19.3K
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...
19.3K
Pyruvate Oxidation01:15

Pyruvate Oxidation

170.3K
After glycolysis, the charged pyruvate molecules enter the mitochondria via active transport and undergo three enzymatic reactions. These reactions ensure that pyruvate can enter the next metabolic pathway so that energy stored in the pyruvate molecules can be harnessed by the cells.
First, the enzyme pyruvate dehydrogenase removes the carboxyl group from pyruvate and releases it as carbon dioxide. The stripped molecule is then oxidized and releases electrons, which are then picked up by NAD+...
170.3K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Messenger RNA-encoded reporters for monitoring cellular stress and bioenergetics.

Scientific reports·2026
Same author

Exploring Replicative Senescence and Oxidative Stress-Induced Remodelling of Mitochondrial-Associated Membranes in Human Skin Fibroblasts.

Biomolecules·2026
Same author

Single-Cell Transcriptomics Reveal Human Skin Aging Pathways.

Journal of cosmetic dermatology·2026
Same author

Toll-like receptor 2 drives liver senescence and fibrosis in aging through gut-derived microbial signaling.

Cellular & molecular biology letters·2026
Same author

Dysregulated Klotho and FGF23 signalling aggravates vascular remodelling in age-related pulmonary hypertension.

Cardiovascular research·2026
Same author

Corrigendum to "Prevention of colitis-induced liver oxidative stress and inflammation in a transgenic mouse model with increased omega-3 polyunsaturated fatty acids" [Redox Biol. 64 (2023) 102803].

Redox biology·2026
Same journal

Corrigendum to: "NO modulates human airway smooth muscle function by altering glucose-6-phosphate dehydrogenase effects on sGC function in asthma" [Redox Biology 95 (2026) 104262].

Redox biology·2026
Same journal

Inhibiting 15-PGDH restores redox homeostasis and confers neuroprotection in Parkinson's disease.

Redox biology·2026
Same journal

Insights into taurine therapy for periodontitis: Targeting osteocyte ferroptosis to mitigate obesity-exacerbated bone damage.

Redox biology·2026
Same journal

Glutathione metabolism-linked ferroptosis in human seminoma: a spatial multi-omics mapping study.

Redox biology·2026
Same journal

Apurinic/apyrimidinic endonuclease 1 prevents oxidative DNA damage in intestinal epithelial cells induced by genotoxic Escherichia coli NC101.

Redox biology·2026
Same journal

Low serum selenium combined with SELENOP-autoantibodies are associated with persistent fatigue after SARS-CoV-2 infection.

Redox biology·2026
See all related articles

Related Experiment Video

Updated: Mar 8, 2026

Author Spotlight: Improved Lipofuscin Models and Quantification of Outer Segment Phagocytosis Capacity in Highly Polarized Human Retinal Pigment Epithelial Cultures
10:39

Author Spotlight: Improved Lipofuscin Models and Quantification of Outer Segment Phagocytosis Capacity in Highly Polarized Human Retinal Pigment Epithelial Cultures

Published on: April 14, 2023

3.3K

Mitochondrial contribution to lipofuscin formation.

Jeannette König1, Christiane Ott1, Martín Hugo1

  • 1Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany.

Redox Biology
|February 5, 2017
PubMed
Summary
This summary is machine-generated.

Mitochondria contribute to lipofuscin accumulation in aging cells. Impaired mitophagy and mitochondrial dysfunction worsen this process, but antioxidants can prevent lipofuscin buildup.

Keywords:
AgingLipofuscinLon proteaseMitochondriaOxidative stressProtein aggregates

More Related Videos

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
09:40

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

12.3K
Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase COX/SDH Double-labeling Histochemistry
06:53

Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase COX/SDH Double-labeling Histochemistry

Published on: November 23, 2011

37.8K

Related Experiment Videos

Last Updated: Mar 8, 2026

Author Spotlight: Improved Lipofuscin Models and Quantification of Outer Segment Phagocytosis Capacity in Highly Polarized Human Retinal Pigment Epithelial Cultures
10:39

Author Spotlight: Improved Lipofuscin Models and Quantification of Outer Segment Phagocytosis Capacity in Highly Polarized Human Retinal Pigment Epithelial Cultures

Published on: April 14, 2023

3.3K
Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
09:40

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

12.3K
Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase COX/SDH Double-labeling Histochemistry
06:53

Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase COX/SDH Double-labeling Histochemistry

Published on: November 23, 2011

37.8K

Area of Science:

  • Cellular Biology
  • Aging Research
  • Mitochondrial Biology

Background:

  • Mitochondria are central to oxidative stress and aging due to reactive oxygen species (ROS) production.
  • Lipofuscin, an autofluorescent aggregate, accumulates in senescent cells, and its formation is hypothesized to involve mitochondria.

Purpose of the Study:

  • To investigate the role of mitochondria in lipofuscinogenesis.
  • To analyze mitochondrial function and lipofuscin levels in young versus senescent cells.
  • To explore the impact of mitochondrial degradation pathways on lipofuscin formation.

Main Methods:

  • Analysis of lipofuscin amounts and mitochondrial function in young and senescent cells.
  • Utilized an aging model and Lon protease-deficient HeLa cells.
  • Assessed the effects of mitophagy impairment, mitochondrial fission inhibition, and mitoTEMPO application.

Main Results:

  • Mitophagy is impaired in senescent cells, leading to increased mitochondrial mass and superoxide production.
  • Inhibition of mitochondrial fission correlates with increased lipofuscin formation.
  • Downregulation of Lon protease is linked to higher lipofuscinogenesis.
  • The antioxidant mitoTEMPO prevented lipofuscin accumulation.

Conclusions:

  • Mitochondrial dysfunction and impaired mitophagy contribute significantly to lipofuscinogenesis in aging.
  • Mitochondrial dynamics, specifically fission, play a role in regulating lipofuscin formation.
  • Targeting mitochondrial processes, such as oxidative stress with antioxidants, can mitigate lipofuscin accumulation.