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Related Concept Videos

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...

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Related Experiment Video

Updated: Jul 4, 2026

Generation of Human Brain Organoids for Mitochondrial Disease Modeling
08:09

Generation of Human Brain Organoids for Mitochondrial Disease Modeling

Published on: June 21, 2021

Biomimetic nanoplatforms modulating mitochondrial pathways in IVDD.

Jian-Bin Guan1,2, Shan-Xi Wang1,2, Ying-Guang Wang1,2

  • 1Department of Spine Surgery, Honghui Hospital, Xi'an Jiaotong University, Xi'an, 710054, China.

Journal of Nanobiotechnology
|July 3, 2026
PubMed
Summary
This summary is machine-generated.

A novel mitochondria-targeted nanoplatform effectively treats intervertebral disc degeneration (IVDD) by reducing oxidative stress and inflammation. This biomimetic approach shows promise for regenerative medicine in degenerative disc diseases.

Keywords:
Biomimetic nanotechnologyCGAS-STING pathwayCellular senescenceIntervertebral disc degenerationMitochondria-targeted nanoparticlesOxidative stress

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An In Vitro Approach to Study Mitochondrial Dysfunction: A Cybrid Model
06:05

An In Vitro Approach to Study Mitochondrial Dysfunction: A Cybrid Model

Published on: March 9, 2022

Area of Science:

  • Biomedical Engineering
  • Nanomedicine
  • Regenerative Medicine

Background:

  • Intervertebral disc degeneration (IVDD) is a major cause of low back pain.
  • Oxidative stress, mitochondrial dysfunction, and inflammation are key contributors to IVDD.
  • Current treatments for IVDD are limited in efficacy and often fail to address underlying pathological mechanisms.

Purpose of the Study:

  • To develop and evaluate a mitochondria-targeted biomimetic nanoplatform (nMitoQ-SNA-CMT) for treating IVDD.
  • To investigate the nanoplatform's effects on mitochondrial function, oxidative stress, mitophagy, and inflammatory signaling in nucleus pulposus cells (NPCs) and an IVDD rat model.

Main Methods:

  • Establishment of rat IVDD and H2O2-induced oxidative stress models in NPCs.
  • Evaluation of nMitoQ-SNA-CMT's impact on mitochondrial function, ROS scavenging, miR-141-3p silencing, UPRmt activation, and mitophagy.
  • Assessment of therapeutic efficacy using molecular, cellular, and histological analyses in vitro and in vivo.

Main Results:

  • nMitoQ-SNA-CMT successfully targeted mitochondria, scavenged ROS, and silenced miR-141-3p, activating SESN2-dependent UPRmt and mitophagy.
  • The nanoplatform reduced mitochondrial DNA release, suppressed cGAS-STING activation, and attenuated NPC senescence, inflammation, and ECM degradation.
  • In IVDD rat models, nMitoQ-SNA-CMT significantly restored disc structure and function, outperforming free MitoQ and non-coated nanoparticles.

Conclusions:

  • nMitoQ-SNA-CMT is a potent and safe therapeutic strategy for IVDD.
  • The nanoplatform effectively regulates mitochondrial oxidative stress, mitophagy, and innate immune activation.
  • nMitoQ-SNA-CMT offers a promising platform for precision nanomedicine in degenerative disc diseases.