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

Nucleotide Excision Repair01:38

Nucleotide Excision Repair

3.4K
DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
3.4K
Mutations01:35

Mutations

33.1K
Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
33.1K
Overview of DNA Repair02:25

Overview of DNA Repair

30.0K
In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
30.0K
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

11.9K
The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
11.9K
Epigenetic Regulation01:37

Epigenetic Regulation

3.0K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
3.0K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.0K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
9.0K

You might also read

Related Articles

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

Sort by
Same author

Environmental high temperature (heat stroke) causes articular cartilage damage in vivo and in vitro.

Ecotoxicology and environmental safety·2024
Same author

Sesquiterpenoids from aged Artemisia argyi and their 3D-QSAR for anti-HBV activity.

Phytochemistry·2023
Same author

Manipulating Cis-Trans Copolymer Chain Conformation to Simultaneously Improve Permittivity and DC Breakdown Strength in Polythiourea.

Macromolecular rapid communications·2023
Same author

Students learning performance prediction based on feature extraction algorithm and attention-based bidirectional gated recurrent unit network.

PloS one·2023
Same author

Integration of metabolomics and transcriptomics reveals metformin suppresses thyroid cancer progression via inhibiting glycolysis and restraining DNA replication.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2023
Same author

Learning based compressive snapshot spectral light field imaging with RGB sensors.

Optics express·2023

Related Experiment Video

Updated: May 27, 2025

Real-time Visualization and Analysis of Chondrocyte Injury Due to Mechanical Loading in Fully Intact Murine Cartilage Explants
08:42

Real-time Visualization and Analysis of Chondrocyte Injury Due to Mechanical Loading in Fully Intact Murine Cartilage Explants

Published on: January 7, 2019

6.8K

Environmental high temperature induced cartilage damage through triggering programmed necrosis mediated by producing

Sun Yingfei1, Yang Feng1, Ma Haoning1

  • 1China-Japan Friendship Hospital, China.

Ecotoxicology and Environmental Safety
|February 16, 2025
PubMed
Summary

Extreme heat causes heat stroke (HS), damaging cartilage and worsening osteoarthritis by inducing chondrocyte senescence and inflammation. Fibroblast growth factor 1 (FGF1) shows promise in treating heat-induced cartilage damage.

Keywords:
AgingChondrocyteHeatstrokeZ-DNA

More Related Videos

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
08:52

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Published on: March 18, 2022

2.9K
Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter
12:15

Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter

Published on: May 29, 2019

8.6K

Related Experiment Videos

Last Updated: May 27, 2025

Real-time Visualization and Analysis of Chondrocyte Injury Due to Mechanical Loading in Fully Intact Murine Cartilage Explants
08:42

Real-time Visualization and Analysis of Chondrocyte Injury Due to Mechanical Loading in Fully Intact Murine Cartilage Explants

Published on: January 7, 2019

6.8K
Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
08:52

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Published on: March 18, 2022

2.9K
Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter
12:15

Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter

Published on: May 29, 2019

8.6K

Area of Science:

  • Environmental Health
  • Cell Biology
  • Rheumatology

Background:

  • Global climate warming poses public health challenges, with extreme heat events increasing heat stroke (HS) incidence.
  • Heat stroke can cause organ damage and death, but its effects on cartilage and osteoarthritis are not fully understood.

Purpose of the Study:

  • To investigate the toxicological effects of heat stroke on chondrocytes and cartilage.
  • To elucidate the molecular mechanisms underlying heat stroke-induced chondrocyte damage and aging.
  • To explore the therapeutic potential of Fibroblast Growth Factor 1 (FGF1) in mitigating heat stroke-induced cartilage damage.

Main Methods:

  • In vitro chondrocyte models and in vivo gene-knockout mouse models were utilized.
  • Assessed chondrocyte proliferation, oxidative stress, inflammation, and senescence markers (p21, p16, p53).
  • Investigated Z-DNA formation, ZBP-1 activation, and the role of FGF1 and the AMPK signaling pathway.

Main Results:

  • Heat stroke significantly reduced chondrocyte proliferation, induced oxidative stress, inflammation, and senescence.
  • Heat stroke triggered Z-DNA formation and ZBP-1-mediated necrosis, leading to cartilage aging and aggravated osteoarthritis in vivo.
  • FGF1 reduced heat stroke-induced chondrocyte damage by activating the AMPK signaling pathway.

Conclusions:

  • Heat stroke induces chondrocyte senescence and exacerbates osteoarthritis through Z-DNA/ZBP-1 pathways.
  • FGF1 demonstrates therapeutic potential for treating heat stroke-related cartilage damage by activating AMPK signaling.