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

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

160
Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates...
160
Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists01:29

Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists

272
Dopamine receptor antagonists, also known as antipsychotic agents, are critical in managing chemotherapy-induced vomiting. These antiemetic agents block dopamine receptors in the chemoreceptor trigger zone (CTZ), inhibiting signal transmission to the vomiting center. Antipsychotic agents encompass phenothiazines (PTZ), butyrophenones, benzamides, and thienobenzodiazepines (Zyprexa), which are utilized for their antiemetic and sedative properties.
Phenothiazines, such as prochlorperazine...
272
Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists01:27

Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists

198
5-HT3 receptor antagonists, such as dolasetron, granisetron (Kytril), ondansetron (Zofran), and palonosetron (Axoli), are crucial in managing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea. These drugs selectively block 5-HT3 receptors in the visceral vagal and spinal afferent nerves, chemoreceptor trigger zone, and the vomiting center. They have a rapid onset of action and can be given as a single dose before chemotherapy. Ondansetron and granisetron, in particular,...
198
Chemotherapy-Induced Nausea and Vomiting: Cannabinoids01:21

Chemotherapy-Induced Nausea and Vomiting: Cannabinoids

237
Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
Two synthetic agonists of THC,...
237
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

4.9K
Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
4.9K
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

13.1K
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...
13.1K

You might also read

Related Articles

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

Sort by
Same author

Hypertension and brain damage: evidence from rodent models.

Laboratory animal research·2026
Same author

Mitochondria-Associated MicroRNAs: Emerging Roles in the Pathogenesis of Parkinson's Disease.

Biomedicines·2026
Same author

Next-Gen Stroke Models: The Promise of Assembloids and Organ-on-a-Chip Systems.

Cells·2025
Same author

Exploring the Antioxidant Roles of Cysteine and Selenocysteine in Cellular Aging and Redox Regulation.

Biomolecules·2025
Same author

Retinal Gatekeepers: Molecular Mechanism and Therapeutic Role of Cysteine and Selenocysteine.

Biomolecules·2025
Same author

The Inflammatory Bridge Between Type 2 Diabetes and Neurodegeneration: A Molecular Perspective.

International journal of molecular sciences·2025

Related Experiment Video

Updated: Jun 27, 2025

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

18.2K

Molecular and Cellular Involvement in CIPN.

Housem Kacem1, Annamaria Cimini1, Michele d'Angelo1

  • 1Department of Life, Health and Environmental Sciences, University of L'Aquila, 67100 L'Aquila, Italy.

Biomedicines
|April 27, 2024
PubMed
Summary
This summary is machine-generated.

Chemotherapy-induced peripheral neuropathy (CIPN) is a common, debilitating side effect of anti-cancer drugs. This review explores the complex mechanisms behind CIPN and highlights the urgent need for effective treatments.

Keywords:
channelschemotherapymechanismsneuroinflammationneuropathy

More Related Videos

Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment
04:48

Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment

Published on: January 7, 2015

7.4K
Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1
09:39

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1

Published on: February 13, 2018

9.5K

Related Experiment Videos

Last Updated: Jun 27, 2025

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

18.2K
Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment
04:48

Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment

Published on: January 7, 2015

7.4K
Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1
09:39

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1

Published on: February 13, 2018

9.5K

Area of Science:

  • Oncology
  • Neuroscience
  • Pharmacology

Background:

  • Chemotherapy-induced peripheral neuropathy (CIPN) is a significant adverse effect of various anti-cancer agents, including taxanes, platinum compounds, vinca alkaloids, and proteasome inhibitors.
  • CIPN manifests as sensory, motor, and autonomic nerve dysfunction, leading to symptoms like pain, numbness, tingling, and weakness, severely impacting patient quality of life.

Purpose of the Study:

  • To provide a comprehensive overview of the current understanding of CIPN.
  • To elucidate the complex biological and molecular mechanisms underlying CIPN.
  • To identify challenges and future directions for CIPN research, including biomarker and therapeutic target development.

Main Methods:

  • Literature review focusing on peer-reviewed articles and clinical studies.
  • Analysis of current knowledge on the pathophysiology of CIPN.
  • Synthesis of information regarding genetic, epigenetic, and environmental factors influencing CIPN.

Main Results:

  • CIPN results from direct nerve damage, oxidative stress, inflammation, DNA damage, microtubule dysfunction, and altered ion channel activity.
  • Individual susceptibility to CIPN is influenced by a combination of genetic, epigenetic, and environmental factors.
  • Current management strategies for CIPN are primarily symptomatic and palliative, with no universally effective treatments or preventative measures.

Conclusions:

  • A deeper understanding of CIPN's cellular and molecular mechanisms is crucial for developing effective interventions.
  • There is a critical need for novel biomarkers and therapeutic targets to prevent or treat CIPN.
  • Further research is required to address the significant unmet need for effective CIPN management in cancer patients.