盖莱克-3标志着容易失败的高缩心脏中的活化巨细胞,并导致心脏功能障碍
Umesh C Sharma1, Saraswati Pokharel, Thomas J van Brakel
1Experimental and Molecular Cardiology Laboratory, Department of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht, The Netherlands. y.pinto@carim.unimaas.nl.
Circulation
|November 3, 2004
概括
在高缩的心脏中,加勒-3的早期增加表明心力衰竭的风险. 这种巨细胞衍生媒介驱动心脏纤维细胞的变化和功能障碍,这表明早期的抗炎疗法至关重要.
科学领域:
- 心血管生物学 心血管生物学
- 炎症研究 炎症研究
- 分子心脏病学分子心脏病学
背景情况:
- 炎症机制和细胞因子与心力衰竭 (HF) 的进展有关.
- 目前尚不清楚这些机制是否在补偿性缩心脏中活跃,并有助于HF发展.
研究的目的:
- 在心力衰竭发作之前,研究心脏缩的早期炎症标志物.
- 确定加勒-3在心脏功能障碍发展中的作用.
主要方法:
- 微阵列分析老鼠心脏的不同程度的缩和心力衰竭.
- 盖列-3与心肌巨细胞的免疫组合化学局部化.
- 在体外研究中,使用心脏纤维细胞上的重组加勒-3进行了研究.
- 在体内研究,包括对健康大鼠输注加勒-3的研究.
- 在人类大动脉狭窄患者中分析心肌盖列-3表达.
主要成果:
- 加勒-3是失败与补偿心脏中表达过度最显著的基因.
- 在从早期高缩阶段迅速发展HF的老鼠中观察到加勒-3的表达增加.
- 加勒-3与激活的巨细胞结合并诱导心脏纤维细胞的增殖和原蛋白的生产.
- 在健康的老鼠中注入加勒-3导致左心室功能障碍和改变原成分.
- 在患有大动脉狭窄和射出分数减少的人类患者中发现了心肌 galectin-3 的升高.
结论:
- 早期加勒-3表达的提升可以识别心脏容易失败.
- 加列-3是一种巨细胞衍生的调解物,促进心脏纤维细胞活性,原沉积和心室功能障碍.
- 针对HF炎症反应的疗法可能需要专注于早期阶段和多种调解剂,如加勒-3.
相关概念视频
Pathophysiology of Heart Failure
Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
Imbalances in Cardiac Output
The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send blood...
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send blood...
Myocarditis I: Introduction
Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
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...
Heart Failure III: Clinical Manifestations
Heart failure (HF) manifests primarily as dyspnea, fatigue, and fluid retention, resulting in peripheral and pulmonary edema. Symptoms may vary depending on which ventricle is more affected, left or right.Left-Sided Heart FailureAlso known as left ventricular failure, this condition results from the left ventricle's inability to fill or eject sufficient blood into the systemic circulation. It leads to pulmonary congestion, which occurs when the left ventricle fails to eject blood effectively...
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...


