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

Necrosis01:16

Necrosis

6.1K
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
6.1K
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

790
Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
790
Overview of Cell Death01:30

Overview of Cell Death

9.1K
Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
9.1K
Inflammatory Bowel Disease V: Surgical Management01:21

Inflammatory Bowel Disease V: Surgical Management

384
Surgical interventions for inflammatory bowel disease (IBD), which includes ulcerative colitis and Crohn's disease, are essential in managing symptoms and addressing complications. The selection of surgical procedures is contingent upon the specific conditions and complications that stem from these illnesses.
Here are some common surgical interventions for IBD:
384
Chronic Bowel Disorders: Introduction01:17

Chronic Bowel Disorders: Introduction

700
Chronic bowel diseases are a group of long-term conditions affecting the digestive tract, characterized by inflammation and damage to the gut lining. These conditions primarily include irritable bowel syndrome and inflammatory bowel disease.
Irritable Bowel Syndrome (IBS) is a common disorder affecting the gastrointestinal tract. The distinctive feature is recurrent abdominal pain associated with altered bowel movements, manifesting as constipation, diarrhea, or fluctuating between both. The...
700
Inflammatory Bowel Disease II: Crohn's Disease01:30

Inflammatory Bowel Disease II: Crohn's Disease

856
Introduction
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
Crohn's disease is a chronic, systemic inflammatory bowel disease (IBD) that predominantly affects the gastrointestinal tract. It is marked by...
856

You might also read

Related Articles

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

Sort by
Same author

The endoplasmic reticulum is a target organelle for trivalent dimethylarsinic acid (DMAIII)-induced cytotoxicity.

Toxicology and applied pharmacology·2012
Same author

(E)-1-{4-[Bis(4-bromo-phen-yl)meth-yl]piperazin-1-yl}-3-(4-eth-oxy-phen-yl)prop-2-en-1-one.

Acta crystallographica. Section E, Structure reports online·2012
Same author

(E)-1-{4-[Bis(4-bromo-phen-yl)meth-yl]piperazin-1-yl}-3-(4-methyl-phen-yl)prop-2-en-1-one.

Acta crystallographica. Section E, Structure reports online·2012
Same author

(E)-3-(1,3-Benzodioxol-5-yl)-1-{4-[bis-(4-meth-oxy-phen-yl)meth-yl]piperazin-1-yl}prop-2-en-1-one.

Acta crystallographica. Section E, Structure reports online·2012
Same author

Economic evaluation of first-line treatments for metastatic renal cell carcinoma: a cost-effectiveness analysis in a health resource-limited setting.

PloS one·2012
Same author

Metabolism studies of casticin in rats using HPLC-ESI-MS(n).

Biomedical chromatography : BMC·2012

Related Experiment Video

Updated: Dec 29, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
04:01

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

Published on: March 15, 2024

1.7K

Ferroptosis involves in intestinal epithelial cell death in ulcerative colitis.

Minyi Xu1, Jin Tao1, Yidong Yang1

  • 1Department of Gastroenterology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.

Cell Death & Disease
|February 5, 2020
PubMed
Summary

Ferroptosis, a regulated cell death, contributes to ulcerative colitis (UC) by inducing intestinal epithelial cell death via ER stress. Nuclear factor kappa Bp65 (NF-κBp65) phosphorylation suppresses this ferroptosis, alleviating UC.

More Related Videos

Author Spotlight: Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids
06:31

Author Spotlight: Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids

Published on: June 2, 2023

1.4K
Author Spotlight: Understanding Cytokine-Induced Cell Death in Intestinal Epithelial Cells Using Human Organoids
10:03

Author Spotlight: Understanding Cytokine-Induced Cell Death in Intestinal Epithelial Cells Using Human Organoids

Published on: August 2, 2024

1.9K

Related Experiment Videos

Last Updated: Dec 29, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
04:01

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

Published on: March 15, 2024

1.7K
Author Spotlight: Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids
06:31

Author Spotlight: Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids

Published on: June 2, 2023

1.4K
Author Spotlight: Understanding Cytokine-Induced Cell Death in Intestinal Epithelial Cells Using Human Organoids
10:03

Author Spotlight: Understanding Cytokine-Induced Cell Death in Intestinal Epithelial Cells Using Human Organoids

Published on: August 2, 2024

1.9K

Area of Science:

  • Cell Biology
  • Gastroenterology
  • Immunology

Background:

  • Ferroptosis is an iron-dependent cell death pathway.
  • Its role in ulcerative colitis (UC) pathogenesis is not well understood.
  • Intestinal epithelial cell (IEC) death is a hallmark of UC.

Purpose of the Study:

  • To investigate ferroptosis involvement in UC, specifically IEC death.
  • To analyze the role of nuclear factor kappa Bp65 subunit (NF-κBp65) in ferroptosis.
  • To explore the therapeutic potential of targeting ferroptosis in UC.

Main Methods:

  • Assessed ferroptosis-related protein expression in human UC samples.
  • Induced experimental colitis using dextran sulfate sodium (DSS).
  • Utilized IEC-specific NF-κBp65-deleted mice (p65IEC-KO) to study NF-κBp65 function.
  • Investigated ferroptosis signaling pathways in vitro and in vivo.

Main Results:

  • Ferroptosis was significantly induced in IECs from UC patients and colitis mice.
  • Ferroptosis in UC is mediated by endoplasmic reticulum (ER) stress signaling.
  • Deletion of IEC NF-κBp65 upregulated ferroptosis and worsened colitis.
  • Phosphorylated NF-κBp65 inhibited ER stress signaling by binding eukaryotic initiation factor 2α.

Conclusions:

  • Ferroptosis contributes to UC via ER stress-mediated IEC death.
  • NF-κBp65 phosphorylation suppresses ER stress-mediated ferroptosis, alleviating UC.
  • Ferroptosis represents a potential therapeutic target for UC.