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

Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants


Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Cholinergic Receptors: Nicotinic01:15

Cholinergic Receptors: Nicotinic

Nicotinic receptors are ligand-gated ion channels that are activated by acetylcholine and nicotine. Upon activation, they cause a rapid increase in the permeability of cells to K+, Na+, and Ca2+, followed by depolarization and excitation. They are in the autonomic ganglia, skeletal neuromuscular junction, CNS, and adrenal medulla.
There are two types of nicotinic receptors: neuromuscular (NM/NM/N1) and neuronal (NN/NN/N2). The two families differ based on their location and selectivity to...
Drugs Acting on Autonomic Ganglia: Blockers01:28

Drugs Acting on Autonomic Ganglia: Blockers

Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups:
Stimulants01:29

Stimulants

Stimulants are substances that enhance neural activity and elevate dopamine levels in the brain, leading to their highly addictive nature. These drugs include cocaine, amphetamines, MDMA, caffeine, and nicotine, each with distinct mechanisms of action and varied health implications.
Cocaine can be administered via snorting, injection, or smoking. It primarily functions by blocking the reuptake of dopamine, resulting in a euphoric high characterized by an intense sensation of happiness and...

You might also read

Related Articles

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

Sort by
Same author

Fluid Shear-Controlled Pro/Anti-Inflammatory Osteomodulatory Construct for Drug-Free Immune Activation Through Cationic Ion Channel Activation.

Advanced healthcare materials·2025
Same author

Effectiveness and Clinical Outcomes of PGT-M Using Karyomapping for Successful Pregnancy and Birth in Various Types of Charcot-Marie-Tooth Disease.

Journal of personalized medicine·2025
Same author

Prevalence of germline <i>BRCA1/2</i> pathogenic variants in unselected Korean patients with HER2-negative metastatic breast cancer: a nationwide prospective study (KCSG BR19-10).

The Lancet regional health. Western Pacific·2025
Same author

2025 Clinical Practice Guidelines for Diabetes Management in Korea: Recommendation of the Korean Diabetes Association.

Diabetes & metabolism journal·2025
Same author

Targeting CD155 in lung adenocarcinoma: A5 nanobody-based therapeutics for precision treatment and enhanced drug delivery.

Signal transduction and targeted therapy·2025
Same author

Interface-Sensitive Charge Storage and Activation Behavior of Mn(1,3,5-Benzenetricarboxylic Acid (BTC))-Derived Mn<sub>3</sub>O<sub>4</sub>/Carbon Cathodes for Aqueous Zinc-Ion Batteries.

Molecules (Basel, Switzerland)·2025
Same journal

Corrigendum to "Adipose stem cells-derived microvesicles and chicken egg-derived exosomes attenuate cardiac ischemia/reperfusion injury through AKT/ERK/Nrf2/HO-1 axis to inhibit apoptosis and inflammation and restore autophagy" [Life Sci. 395 (2026) 124364].

Life sciences·2026
Same journal

MAGED1 stabilizes NEUROD1 to promote Per3 expression in the pineal gland.

Life sciences·2026
Same journal

TNF-centered network pharmacology and molecular modeling of selected Andrographis paniculata compounds in hypertension.

Life sciences·2026
Same journal

Retraction notice to "Beneficial effect of Calculus Bovis Sativus on 17α-ethynylestradiol-induced cholestasis in the rat" [Life Sci. 113 (2014) 22-30].

Life sciences·2026
Same journal

Soluble PD-1 drives renal fibrosis in CKD by disrupting immune homeostasis: Therapeutic mitigation via a targeted sPD-1 sequestration strategy.

Life sciences·2026
Same journal

METTL1 promotes hepatic steatosis by mediating m<sup>7</sup>G modification of ALOX15B mRNA.

Life sciences·2026
See all related articles

Related Experiment Video

Updated: May 20, 2026

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
08:19

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

Published on: July 20, 2019

Nicotine and pathological angiogenesis.

Jieun Lee1, John P Cooke

  • 1Division of Cardiovascular Medicine, Stanford University School of Medicine, USA.

Life Sciences
|July 17, 2012
PubMed
Summary
This summary is machine-generated.

Nicotine promotes pathological angiogenesis by activating endothelial nicotinic acetylcholine receptors (nAChR), contributing to smoking-related diseases like cancer and macular degeneration. Targeting these receptors may offer new therapeutic strategies.

More Related Videos

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies
09:03

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies

Published on: June 30, 2023

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition
06:12

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition

Published on: March 3, 2023

Related Experiment Videos

Last Updated: May 20, 2026

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
08:19

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

Published on: July 20, 2019

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies
09:03

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies

Published on: June 30, 2023

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition
06:12

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition

Published on: March 3, 2023

Area of Science:

  • Cardiovascular Research
  • Oncology
  • Ophthalmology

Background:

  • Pathological angiogenesis is implicated in major diseases like carcinoma, atherosclerosis, and age-related macular degeneration.
  • Nicotine, a key component of tobacco, has been investigated for its potential role in promoting angiogenesis.

Purpose of the Study:

  • To review the literature on nicotine's effect on angiogenesis.
  • To elucidate the role of endothelial nicotinic acetylcholine receptors (nAChR) in nicotine-induced pathological angiogenesis.
  • To explore potential therapeutic targets for angiogenesis-related diseases.

Main Methods:

  • Extensive literature review focusing on nicotine's impact on angiogenesis.
  • Analysis of in vitro studies on endothelial cell behavior (migration, proliferation, survival, tube formation, nitric oxide production).
  • Examination of pre-clinical models of angiogenesis-related disorders.

Main Results:

  • Nicotine induces pathological angiogenesis at concentrations relevant to smokers.
  • Nicotine promotes endothelial cell functions crucial for angiogenesis in vitro.
  • Nicotine stimulates endothelial nAChRs, predominantly α7 homomeric type, to drive angiogenic processes.
  • Synergistic interactions observed between nAChRs and angiogenic growth factor receptors.

Conclusions:

  • Endothelial nAChRs play a significant role in nicotine-induced pathological angiogenesis.
  • Mechanisms elucidated provide insights into tobacco-related diseases.
  • Findings suggest potential for novel therapies targeting nAChRs for diseases with aberrant angiogenesis.