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

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

15.3K
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...
15.3K
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

8.4K
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,...
8.4K
The Electron Transport Chain01:30

The Electron Transport Chain

18.1K
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...
18.1K

You might also read

Related Articles

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

Sort by
Same author

Hydrogel-Based Systems in Intrauterine Adhesions: Bridging the Gap from Bench to Bedside.

Advanced healthcare materials·2026
Same author

Bioresponsive microneedle stent provides anastomosis and postoperative adjuvant therapy in preclinical resectable intestinal diseases.

Science translational medicine·2026
Same author

Mechanical movements generated by movable lipids break endosomal barriers for enhanced mRNA therapeutics.

Science advances·2026
Same author

Deep learning for radiographic differentiation between lateral malleolar avulsion fractures and subfibular ossicles.

iScience·2026
Same author

Advances in artificial metabzymes for molecular metabolism restoration in aging-related diseases.

Chemical communications (Cambridge, England)·2026
Same author

Self-assembly for cuproptosis-based cancer therapy and imaging.

Chemical Society reviews·2026

Related Experiment Video

Updated: Oct 18, 2025

Author Spotlight: Bidirectional Mitochondrial Transfer between MSCs and Retinal Pigment Epithelium Cells — Pathways and In Vivo Challenges
06:50

Author Spotlight: Bidirectional Mitochondrial Transfer between MSCs and Retinal Pigment Epithelium Cells — Pathways and In Vivo Challenges

Published on: October 4, 2024

1.1K

Iron oxide nanoparticles augment the intercellular mitochondrial transfer-mediated therapy.

Ting Huang1, Tianyuan Zhang1,2, Xinchi Jiang1,2

  • 1College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China.

Science Advances
|September 29, 2021
PubMed
Summary

Iron oxide nanoparticles enhance mitochondrial transfer from stem cells to injured cells, improving disease treatment. This method shows promise for restoring cell energy and mitigating fibrosis with good safety.

More Related Videos

Polyethyleneimine-coated Iron Oxide Nanoparticles as a Vehicle for the Delivery of Small Interfering RNA to Macrophages In Vitro and In Vivo
09:36

Polyethyleneimine-coated Iron Oxide Nanoparticles as a Vehicle for the Delivery of Small Interfering RNA to Macrophages In Vitro and In Vivo

Published on: February 5, 2019

8.9K
MitoCeption: Transferring Isolated Human MSC Mitochondria to Glioblastoma Stem Cells
11:13

MitoCeption: Transferring Isolated Human MSC Mitochondria to Glioblastoma Stem Cells

Published on: February 22, 2017

13.2K

Related Experiment Videos

Last Updated: Oct 18, 2025

Author Spotlight: Bidirectional Mitochondrial Transfer between MSCs and Retinal Pigment Epithelium Cells — Pathways and In Vivo Challenges
06:50

Author Spotlight: Bidirectional Mitochondrial Transfer between MSCs and Retinal Pigment Epithelium Cells — Pathways and In Vivo Challenges

Published on: October 4, 2024

1.1K
Polyethyleneimine-coated Iron Oxide Nanoparticles as a Vehicle for the Delivery of Small Interfering RNA to Macrophages In Vitro and In Vivo
09:36

Polyethyleneimine-coated Iron Oxide Nanoparticles as a Vehicle for the Delivery of Small Interfering RNA to Macrophages In Vitro and In Vivo

Published on: February 5, 2019

8.9K
MitoCeption: Transferring Isolated Human MSC Mitochondria to Glioblastoma Stem Cells
11:13

MitoCeption: Transferring Isolated Human MSC Mitochondria to Glioblastoma Stem Cells

Published on: February 22, 2017

13.2K

Area of Science:

  • Cell biology
  • Nanomedicine
  • Regenerative medicine

Background:

  • Mitochondrial transfer between cells protects injured cells.
  • Current methods lack efficiency and selectivity for therapeutic use.

Purpose of the Study:

  • To investigate iron oxide nanoparticles (IONPs) for enhanced intercellular mitochondrial transfer.
  • To improve the efficiency and selectivity of mitochondrial transfer from human mesenchymal stem cells (hMSCs) to diseased cells.

Main Methods:

  • Utilized IONPs to engineer hMSCs for augmented mitochondrial transfer.
  • Investigated the role of connexin 43–containing gap junctional channels.
  • Evaluated therapeutic efficacy in a mouse model of pulmonary fibrosis.

Main Results:

  • IONPs selectively enhanced mitochondrial transfer from hMSCs to diseased cells.
  • IONP-induced gap junction formation was key to improved transfer.
  • IONP-engineered hMSCs significantly mitigated pulmonary fibrosis progression in mice.
  • No serious safety issues were identified.

Conclusions:

  • IONPs offer a method to improve efficiency and selectivity of mitochondrial transfer.
  • This approach holds potential for treating diseases by restoring mitochondrial function.
  • IONP-mediated stem cell therapy presents a safe and effective strategy for fibrotic diseases.