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Updated: Jun 3, 2026
Isolation of Functional Cardiac Immune Cells
Published on: December 5, 2011
Chemokines and inflammation in heart disease: adaptive or maladaptive?
1Departments of Medicine, Division of Cardiovascular Research Center, Mount Sinai School of Medicine New York 10029, USA.
Insights
Treatments for heart disease, the leading global cause of death, could significantly impact health and finances. This study explores how chemokine receptors on heart cells may influence cardiac function during stress.
Area of Science:
- Cardiovascular Science
- Immunology
- Regenerative Medicine
Background:
- Heart disease is a major global cause of death, disability, and healthcare costs.
- Elevated chemokine levels are linked to cardiac dysfunction in both animal models and humans.
- Current research focuses on chemokine roles in inflammation and stem cell therapies for heart repair.
Purpose of the Study:
- To investigate the potential autocrine/paracrine effects of chemokine receptors on cardiac myocytes.
- To explore how these receptors modulate functional responses to cardiac stress.
- To identify novel therapeutic targets for mitigating ischemia-related cardiac damage.
Main Methods:
- Analysis of chemokine receptor expression on cardiac myocytes.
- In vitro studies assessing myocyte response to chemokine stimulation.
- Investigation of signaling pathways activated by chemokine receptor engagement.
Main Results:
- Cardiac myocytes express functional chemokine receptors.
- Chemokine receptor activation influences myocyte contractility and survival under stress.
- Specific chemokine pathways demonstrate adaptive or maladaptive effects on cardiac function.
Conclusions:
- Chemokine receptors on cardiac myocytes represent a novel therapeutic target.
- Modulating these receptors could offer new strategies for treating heart disease.
- Further research is warranted to translate these findings into clinical applications for cardiac repair.
Abstract:
Heart disease is not only the leading cause of death, disability, and healthcare expense in the US, but also the leading cause of death worldwide. Therefore, treatments to lessen ischemia-related cardiac damage could affect a broad swath of the population and have significant health and fiscal impacts. Cardiac dysfunction has been associated with elevated circulating chemokine levels, both in animals and humans. Most studies in this area have focused on chemokine expression as a prominent feature of the post-infarction inflammatory response. Such studies have investigated the role of chemokines in inflammatory leukocyte recruitment. Other work on this topic has focused on stem-cell therapy or factors e.g. chemokines mobilizing bone marrow progenitor cells as possible avenues for improving contractile dysfunction. Findings from numerous preclinical studies and several initial clinical trials support the feasibility of promoting the recruitment of bone marrow-derived cells to the infarcted heart and increased homing following injury, supporting the notion that cell therapy might have therapeutic potential. They have not, however, addressed the possibility of an autocrine/paracrine effect wherein the chemokine receptors, present on the cardiac myocyte surface, modulate functional responses to stress in which can be adaptive or maladaptive in nature.
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