Related Experiment Video

Updated: Jul 15, 2026

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
07:14

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

Plasma level of mitochondrial coupling factor 6 increases in patients with coronary heart disease

San Bao Chai1, Yong Ming Hui, Xue Min Li

  • 1Department of Cardiovascular Disease, Beijing Fengtai Hospital, Beijing, PR China. chaisb@126.com

Circulation Journal : Official Journal of the Japanese Circulation Society
|April 26, 2007
PubMed

Insights

Plasma levels of coupling factor 6 (CF6) were elevated in coronary heart disease patients, while prostacyclin levels decreased. Increased CF6 may contribute to reduced prostacyclin, suggesting CF6 as a potential risk factor for heart disease.

Area of Science:

  • Cardiovascular Medicine
  • Biochemistry
  • Medical Research

Background:

  • Coronary heart disease (CHD) is associated with altered vascular function.
  • Prostacyclin plays a crucial role in maintaining vascular homeostasis.
  • Coupling factor 6 (CF6) is identified as a novel endogenous inhibitor of prostacyclin.

Purpose of the Study:

  • To investigate alterations in plasma levels of CF6 in patients with coronary heart disease.
  • To determine the relationship between CF6 levels and prostacyclin levels in CHD patients.
  • To assess the impact of percutaneous transluminal coronary angioplasty (PTCA) and stent therapy on CF6 and prostacyclin levels.

Main Methods:

  • Radioimmunoassay was used to measure plasma levels of CF6 and 6-keto-prostaglandin F(1a) (a prostacyclin metabolite).
  • Study included 35 patients with CHD and 20 age-matched healthy controls.
  • Measurements were taken before and after PTCA and stent therapy in CHD patients.

Main Results:

  • Plasma CF6 levels were significantly higher in CHD patients compared to controls (254.1 vs 219.4 pg/ml).
  • Plasma 6-keto-PGF(1a) levels were significantly lower in CHD patients compared to controls (23.4 vs 26.1 pg/ml).
  • Following PTCA and stent therapy, CF6 levels increased by 30% and 6-keto-PGF(1a) levels decreased by 42%.

Conclusions:

  • Elevated CF6 levels may contribute to the reduced prostacyclin levels observed in patients with coronary heart disease.
  • CF6 levels increase further after PTCA and stent therapy, exacerbating prostacyclin reduction.
  • CF6 is proposed as a potential risk factor for coronary heart disease with significant clinical implications.
Abstract

More Related Videos

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle09:40

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

Related Concept Videos

Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

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...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Coronary Artery Disease III: Clinical Manifestations01:30

Coronary Artery Disease III: Clinical Manifestations

Coronary Artery Disease (CAD) is a primary health risk worldwide, leading to significant morbidity and mortality. The condition arises from the buildup of atherosclerotic plaques within the coronary arteries, resulting in diminished blood supply to the heart muscle.The clinical manifestations of CAD vary widely, from asymptomatic stages to severe, life-threatening conditions. Understanding these manifestations is crucial for early diagnosis and effective management.Angina Pectoris: The Warning...
Acute Coronary Syndrome III: Diagnostic Studies01:30

Acute Coronary Syndrome III: Diagnostic Studies

Diagnosing acute coronary syndrome or ACS begins with a thorough patient history. Notable symptoms include central, crushing chest pain radiating to the left arm, neck, jaw, or back, along with shortness of breath, sweating (diaphoresis), nausea, vomiting, dizziness, and palpitations.It is crucial to note any history of cardiac illnesses and assess risk factors, including age, gender, smoking, hypertension, diabetes, hyperlipidemia, and a sedentary lifestyle.During physical examination, vital...
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...