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

The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Overview of Cell Death01:30

Overview of Cell Death

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 20th century...

You might also read

Related Articles

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

Sort by
Same author

To β or not to β: think zinc (again)!

Cell research·2026
Same author

Mitochondrial Cell-Type-Specific Profiling: Differential Function of Mesophyll and Guard Cells is Reflected by Their Mitochondrial Proteome.

Physiologia plantarum·2025
Same author

The Hippo terminal effector YAP boosts enterovirus replication in type 1 diabetes.

Nature communications·2025
Same author

Multi-Target Modulation of Polyphenols in Diabetic Kidney Disease Therapeutics: A Comprehensive Review.

Food science & nutrition·2025
Same author

Joint analysis of the nPOD-Virus Group data: the association of enterovirus with type 1 diabetes is supported by multiple markers of infection in pancreas tissue.

Diabetologia·2025
Same author

The adult table: Chronic intermittent fasting improves β cell health only in adults.

Cell reports·2025

Related Experiment Video

Updated: Jun 6, 2026

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
12:12

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes

Published on: June 16, 2011

CXCL10- a path to β-cell death.

Federico Paroni1, Erna Domsgen, Kathrin Maedler

  • 1Centre for Biomolecular Interactions Bremen, University of Bremen, Germany.

Islets
|November 25, 2010
PubMed
Summary

The chemokine CXCL10 triggers beta-cell apoptosis via Toll-like receptor 4, offering new therapeutic targets for diabetes. This research identifies a key pathway in beta-cell destruction and disease progression.

Area of Science:

  • Immunology
  • Endocrinology
  • Cell Biology

Background:

  • Beta-cell dysfunction and apoptosis are central to type 1 and type 2 diabetes.
  • Cytokines and chemokines are implicated in immune responses against beta-cells.

Purpose of the Study:

  • To investigate the role of chemokine CXCL10 in beta-cell destruction.
  • To identify the receptor and signaling pathway for CXCL10-induced beta-cell apoptosis.

Main Methods:

  • Analysis of immune responses targeting beta-cells.
  • Identification of CXCL10 as a key chemokine.
  • Characterization of Toll-like receptor 4 (TLR4) as the CXCL10 receptor.

Main Results:

  • CXCL10 actively contributes to beta-cell destruction.

More Related Videos

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
08:32

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain

Published on: January 4, 2018

Related Experiment Videos

Last Updated: Jun 6, 2026

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
12:12

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes

Published on: June 16, 2011

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
08:32

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain

Published on: January 4, 2018

  • TLR4 is identified as the functional receptor for CXCL10 on beta-cells.
  • A novel pathway for beta-cell apoptosis induction via CXCL10/TLR4 is established.

    • Conclusions:

    • The CXCL10/TLR4 axis represents a significant pathway in beta-cell failure.
    • Targeting this pathway may offer new therapeutic strategies for diabetes management.
    • Understanding this mechanism is crucial for combating diabetes onset and progression.