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Related Experiment Video

Updated: Jun 26, 2026

Detecting Establishment of Shared Blood Supply in Parabiotic Mice by Caudal Vein Glucose Injection

Detecting Establishment of Shared Blood Supply in Parabiotic Mice by Caudal Vein Glucose Injection

Published on: February 6, 2020

CHIP In cardiovascular and immune ageing.

Harish C Chandramoorthy¹, Muhammad Afzal², Haider Ali³

¹Department of Microbiology & Clinical Parasitology, College of Medicine, Stem Cell Research Lab, Medical and Biological Sciences Unit, Central Core Research Laboratories, King Khalid University, Abha, Saudi Arabia.

Ageing Research Reviews

|June 24, 2026

Summary

This summary is machine-generated.

Clonal hematopoiesis of indeterminate potential (CHIP) is linked to aging and increased cardiovascular risk. Larger clone sizes amplify this risk, highlighting CHIP as a key factor in age-related diseases.

Keywords:

CHIP Cardiovascular Aging Immune Aging Inflammaging NLRP3 inflammasome VAF

Related Experiment Videos

Last Updated: Jun 26, 2026

Detecting Establishment of Shared Blood Supply in Parabiotic Mice by Caudal Vein Glucose Injection

Detecting Establishment of Shared Blood Supply in Parabiotic Mice by Caudal Vein Glucose Injection

Published on: February 6, 2020

Area of Science:

Hematology
Genetics
Cardiovascular Medicine

Background:

Clonal hematopoiesis of indeterminate potential (CHIP) involves blood cell clone proliferation with driver mutations (e.g., DNMT3A, TET2) without malignancy.
CHIP incidence increases with age and is associated with cardiovascular and immune system aging.

Purpose of the Study:

To review the epidemiology, pathophysiology, and clinical utility of CHIP.
To discuss the association of CHIP with cardiovascular aging, inflammaging, and somatic mosaicism.

Main Methods:

Review of prospective cohort studies and experimental evidence.
Analysis of genetic drivers, clone size (VAF), and associated molecular pathways (e.g., NLRP3, IL-1β, IL-6).

Main Results:

CHIP significantly elevates risks for myocardial infarction, stroke, and heart failure (1.4-2.0-fold increase).
Larger clone size (VAF) correlates with higher risk.
Proinflammatory myeloid reprogramming and endothelial dysfunction are linked to CHIP-associated gene mutations.

Conclusions:

CHIP is a significant factor in age-related cardiovascular and immune dysfunction.
Further genotype- and VAF-stratified trials are needed to clarify causation and optimize treatment strategies for CHIP.