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

Skeleton and Calcium Homeostasis01:21

Skeleton and Calcium Homeostasis

5.1K
Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
5.1K
Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

3.5K
Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
3.5K
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

5.4K
Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
5.4K
Bone Disorders01:29

Bone Disorders

4.2K
Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
4.2K
Role of Vitamins in Maintaining Bone Health01:25

Role of Vitamins in Maintaining Bone Health

3.9K
The growth and maintenance of bone are regulated by a combination of nutritional factors, including vitamins, such as vitamin A, B12, C, D, and K.
Vitamin A
Vitamin A is involved in the process of bone remodeling. Retinoic acid, the active metabolite of Vitamin A, has nuclear receptors in osteoblasts and osteoclasts, which are involved in bone remodeling.
Vitamin B12
Vitamin B12 acts as a cofactor during the formation of osteoblast-related proteins, such as osteocalcin. Vitamin B12 plays a role...
3.9K
Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

3.4K
Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
3.4K

You might also read

Related Articles

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

Sort by
Same author

PIP<sub>2</sub> corrects an endothelial Piezo1 channelopathy.

Proceedings of the National Academy of Sciences of the United States of America·2025
Same author

Systemic Piezo1 activation improves cerebrovascular function in Alzheimer's disease.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2025
Same author

Role of S1P- and Rho-kinase signalling in age-related myogenic tone deficiency in murine resistance arteries.

Experimental physiology·2025
Same author

VasoTracker 2: Open-source software and hardware for tracking blood vessel diameter and assessing vascular function.

The Journal of physiology·2025
Same author

Brain Capillary Ion Channels: Physiology and Channelopathies.

Physiology (Bethesda, Md.)·2025
Same author

Estrogen Enhances SK Channel Activity to Limit Hippocampal Arteriole Constriction.

Circulation research·2025

Related Experiment Video

Updated: Oct 15, 2025

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro
11:30

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro

Published on: June 2, 2022

2.1K

Vascular calcium signalling and ageing.

Osama F Harraz1,2, Lars Jørn Jensen3

  • 1Department of Pharmacology, Larner College of Medicine, University of Vermont, Burlington, Vermont, USA.

The Journal of Physiology
|October 27, 2021
PubMed
Summary

Ageing disrupts cellular calcium (Ca2+) signalling in vascular cells, impacting blood pressure and cardiovascular health. Understanding these Ca2+ changes is crucial for preventing age-related vascular dysfunction.

Keywords:
ageingblood flow dysregulationcalcium signallingendotheliumhypertensionvascular dysfunctionvascular smooth muscle

More Related Videos

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
08:43

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Published on: May 31, 2016

19.8K
Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
05:47

Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro

Published on: May 10, 2021

4.2K

Related Experiment Videos

Last Updated: Oct 15, 2025

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro
11:30

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro

Published on: June 2, 2022

2.1K
Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
08:43

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Published on: May 31, 2016

19.8K
Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
05:47

Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro

Published on: May 10, 2021

4.2K

Area of Science:

  • Cardiovascular Physiology
  • Cellular Biology
  • Aging Research

Background:

  • Cellular calcium (Ca2+) dynamics are critical for vascular smooth muscle cell (SMC) and endothelial cell (EC) function.
  • Ageing is a significant risk factor for cardiovascular diseases, yet its specific effects on vascular Ca2+ signalling remain understudied.

Purpose of the Study:

  • To review and synthesize current literature on age-related alterations in vascular Ca2+ signalling.
  • To correlate these signalling changes with vascular structure, function, and blood pressure regulation.

Main Methods:

  • Literature review focusing on studies investigating age-related changes in vascular Ca2+ signalling.
  • Analysis of findings related to SMC and EC Ca2+ handling, ion channels, and intracellular stores.

Main Results:

  • Ageing impairs vascular tone via altered expression/activity of SMC ion channels (e.g., voltage-gated Ca2+ channels, Ca2+-activated K+ channels, TRPC6).
  • Reduced intracellular Ca2+ store handling and increased mitochondrial Ca2+ uptake contribute to SMC hypercontractility and oxidative stress in ageing.
  • Ageing affects EC Ca2+ transients and the EC-SMC interface, impacting vasodilatation and vascular structure.

Conclusions:

  • Altered Ca2+ signalling in vascular cells contributes to blood pressure dysregulation and impaired organ blood flow in ageing.
  • Targeting age-induced Ca2+ signalling deficits is essential to mitigate vascular ageing and cardiovascular disease risk.