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

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

2
Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
2
Hematopoiesis01:21

Hematopoiesis

5.1K
The process of blood cell formation is called hematopoiesis. Hematopoiesis starts early during development, on the seventh day of embryogenesis. This phase of hematopoiesis is called the primitive wave, wherein the extraembryonic yolk sac allows the production of erythroid cells and endothelial cells from a common precursor called hemangioblast. The erythroid cells provide oxygen to support the growth of the rapidly dividing embryo. Hemangioblasts later develop into hematopoietic stem cells or...
5.1K
Multipotency of Hematopoietic Stem Cells01:19

Multipotency of Hematopoietic Stem Cells

3.0K
The hematopoietic stem cells or HSCs are multipotent, meaning they can differentiate and give rise to all blood and immune cells. HSCs are maintained in the quiescent stage until an external stimulus initiates their differentiation. The multipotent HSCs exist as two heterogeneous populations, long-term repopulating cells (LTRC) and short-term repopulating cells (STRC). The two HSC populations have different surface markers or receptors and are classified based on quiescence and long-term...
3.0K
Regulation of Hematopoietic Stem Cells01:01

Regulation of Hematopoietic Stem Cells

3.2K
All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
3.2K
Production of Formed Elements01:34

Production of Formed Elements

1.3K
Hemangioblasts are multipotent stem cells originating from the mesoderm. They give rise to hematopoietic stem cells (HSCs), which undergo hematopoiesis to produce all the formed elements of blood. This process is regulated by a complex network of hematopoietic growth factors, including transcription factors, growth factors, and cytokines. These factors stimulate the HSCs to divide and differentiate, though some HSCs remain undifferentiated to maintain a self-renewing pool.
Most HSCs commit to...
1.3K
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

3
Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
3

You might also read

Related Articles

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

Sort by
Same author

Utility of genetic screening for the prediction of severe arrhythmic outcomes in mitral valve prolapse.

medRxiv : the preprint server for health sciences·2026
Same author

Clonal hematopoiesis of indeterminate potential and heart disease: What every internist needs to know.

Cleveland Clinic journal of medicine·2026
Same author

Gamut of Patients Referred to Cardiology for Question of Clonal Hematopoiesis.

Circulation. Genomic and precision medicine·2026
Same author

Wondering Y: How Might Loss of the Y Chromosome Promote Cardiovascular Disease in Aging Men?

Journal of the American College of Cardiology·2026
Same author

Genomic and transcriptomic analyses of aortic stenosis enhance therapeutic target discovery and disease prediction.

Nature genetics·2025
Same author

Incorporating Management of Clonal Hematopoiesis of Indeterminate Potential Into Cardiovascular Practice.

Circulation·2025

Related Experiment Video

Updated: Jun 11, 2025

Bone Marrow Transplantation Procedures in Mice to Study Clonal Hematopoiesis
08:00

Bone Marrow Transplantation Procedures in Mice to Study Clonal Hematopoiesis

Published on: May 26, 2021

12.4K

Clonal hematopoiesis and atherosclerosis.

Ohad Oren1, Aeron M Small2, Peter Libby2

  • 1Division of Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

The Journal of Clinical Investigation
|October 1, 2024
PubMed
Summary
This summary is machine-generated.

Clonal hematopoiesis of indeterminate potential (CHIP), common in aging, is a significant risk factor for cardiovascular disease beyond cancer risk. Certain CHIP mutations accelerate atherosclerosis through distinct inflammatory pathways, guiding personalized therapies.

More Related Videos

Lentiviral CRISPR/Cas9-Mediated Genome Editing for the Study of Hematopoietic Cells in Disease Models
08:14

Lentiviral CRISPR/Cas9-Mediated Genome Editing for the Study of Hematopoietic Cells in Disease Models

Published on: October 3, 2019

12.1K
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

13.1K

Related Experiment Videos

Last Updated: Jun 11, 2025

Bone Marrow Transplantation Procedures in Mice to Study Clonal Hematopoiesis
08:00

Bone Marrow Transplantation Procedures in Mice to Study Clonal Hematopoiesis

Published on: May 26, 2021

12.4K
Lentiviral CRISPR/Cas9-Mediated Genome Editing for the Study of Hematopoietic Cells in Disease Models
08:14

Lentiviral CRISPR/Cas9-Mediated Genome Editing for the Study of Hematopoietic Cells in Disease Models

Published on: October 3, 2019

12.1K
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

13.1K

Area of Science:

  • Hematology
  • Cardiovascular Medicine
  • Genetics

Background:

  • Clonal hematopoiesis of indeterminate potential (CHIP) involves somatic mutations in leukemia driver genes, creating mutant cell clones in peripheral blood.
  • CHIP is an emerging, common, age-related risk factor for atherosclerosis, contributing to excess mortality beyond hematologic malignancy risk.

Purpose of the Study:

  • To investigate the causal role of CHIP mutations in accelerated atherosclerosis.
  • To explore how different CHIP-associated mutations differentially impact atherosclerotic events and pathophysiology.
  • To understand the implications for targeted therapies and personalized medicine.

Main Methods:

  • Analysis of experimental evidence linking CHIP mutations to atherosclerosis.
  • Comparative assessment of atherogenicity across different CHIP mutation types (e.g., DNMT3a vs. TET2/JAK2).

Main Results:

  • Specific CHIP mutations are causally linked to accelerated atherosclerosis.
  • CHIP due to TET2 or JAK2 mutations promotes atherosclerosis via inflammation, unlike DNMT3a mutations.
  • CHIP's cardiovascular risk varies based on the underlying genetic driver mutation.

Conclusions:

  • CHIP is a significant driver of cardiovascular disease, with distinct pathogenic mechanisms based on mutation type.
  • Understanding these mechanisms opens avenues for targeted therapies in CHIP patients.
  • This research advances personalized medicine approaches for managing CHIP-associated cardiovascular risk.