Meox1通过Cthrc1/p-Smad2/3信号传输促进心脏纤维化和心肌梗塞后的病态重塑
Mian Zhang1,2, Xiao-Wen Meng1,2, Yu-Fan Yang1,2
1Department of Anesthesiology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China.
International journal of biological sciences
|December 9, 2025
概括
介质基因母体盒1 (Meox1) 通过激活含有1 (Cthrc1) 和Smad2/3.3.2的原三环重复激活心肌梗塞后的心脏纤维化. 抑制Meox1可以治疗心脏衰竭后的心脏病发作.
科学领域:
- 心血管生物学 心血管生物学
- 分子心脏病学分子心脏病学
- 纤维化研究 纤维化研究
背景情况:
- 心肌梗塞 (MI) 导致心脏纤维化,心室重塑和心力衰竭.
- 梅基母体盒1 (Meox1) 是已知的纤维细胞激活剂,但其在MI诱导纤维化中的作用尚不清楚.
研究的目的:
- 调查Meox1在心脏纤维化和心脏中风后重塑中的作用.
- 在这个过程中阐明Meox1的潜在分子机制.
主要方法:
- 在MI的小鼠模型和用TGF-β1.1.刺激的初级心脏纤维细胞 (CFs) 中分析了Meox1的表达.
- 在CF和体内模型中,Meox1被击倒或过度表达.
- 评估了含有1 (Cthrc1) 和Smad2/3酸化的原三环重复.
主要成果:
- 在MI后的激活纤维细胞 (肌纤维细胞,Myofbs) 和TGF-β1刺激时,Meox1的表达增加.
- Meox1倒置减弱心脏纤维化,不良重塑,心脏功能改善后MI.
- 通过转录激活Cthrc1,Meox1促进了CFs的激活,增殖,迁移和纤维化基因表达,从而导致Smad2/3酸化.
结论:
- 梅奥克斯1在促进心脏纤维化和心脏衰竭后心脏病发作中发挥着关键作用.
- 这种Meox1/Cthrc1/p-Smad2/3通路介导着CFs转化为Myofbs.
- 这一途径代表了治疗心脏纤维化和心脏病发作患者重塑的潜在治疗标.
更多相关视频
09:16Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
7.7K
09:29An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice
Published on: July 14, 2023
1.2K
相关概念视频
01:21Myocarditis I: Introduction
343
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...
343
01:29Cardiomyopathy III: Hypertrophic Cardiomyopathy
374
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...
374
01:29Heart Failure II: Pathophysiology
685
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...
685
01:17Pathophysiology of Heart Failure
2.7K
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...
2.7K
01:30Cardiomyopathy II: Dilated Cardiomyopathy
447
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,...
447