Jove
Visualize
联系我们

相关概念视频

Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

200
Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
200
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

149
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...
149
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

152
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,...
152
Cardiomyopathy I: Introduction and Classification01:25

Cardiomyopathy I: Introduction and Classification

215
Cardiomyopathy, or CMP, is a group of diseases affecting the myocardial structure, impairing its ability to pump blood effectively. This condition can lead to arrhythmias, heart failure, or sudden cardiac death.Cardiomyopathies are classified into primary and secondary categories:Primary Cardiomyopathy refers to conditions involving only the heart muscle that are often idiopathic (of unknown cause) or genetic. They primarily affect the myocardium without the involvement of other systemic...
215
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

188
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...
188
Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

124
Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
124
JoVE
x logofacebook logolinkedin logoyoutube logo
关于 JoVE
概览领导团队博客JoVE 帮助中心
作者
出版流程编辑委员会范围与政策同行评审常见问题投稿
图书馆员
用户评价订阅访问资源图书馆顾问委员会常见问题
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experiments存档
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教师资源中心教师网站
使用条款与条件
隐私政策
政策
  1. 首页
  2. 心肌细胞克鲁佩尔样因子5促进了de Novo胺生物合成,并有助于缺血性心肌病的奇特重塑
  1. 首页
  2. 心肌细胞克鲁佩尔样因子5促进了de Novo胺生物合成,并有助于缺血性心肌病的奇特重塑

相关实验视频

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
09:16

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

7.5K

心肌细胞克鲁佩尔样因子5促进了De Novo胺生物合成,并有助于缺血性心肌病的奇特重塑

Matthew Hoffman1, Dimitra Palioura1, Ioannis D Kyriazis1

  • 1Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA (M.H., D.P., I.D.K., C.M., S.R., E.G., R.K., K.D.).

Circulation
|January 12, 2021

在PubMed 上查看摘要

概括
此摘要是机器生成的。

在心力衰竭中Kryppel类因子 (KLF) 5升高,并促进胺的积累. 在患有心肌梗塞的小鼠中抑制KLF5改善了心脏功能和降低了胺水平,突出显示KLF5是治疗点.

关键词:
心肌疾病化物心脏衰竭心肌缺血症

更多相关视频

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
11:00

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

Published on: September 18, 2017

10.4K
Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
10:21

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix

Published on: June 14, 2016

10.4K

相关实验视频

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
09:16

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

7.5K
Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
11:00

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

Published on: September 18, 2017

10.4K
Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
10:21

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix

Published on: June 14, 2016

10.4K

科学领域:

  • 心脏病学
  • 分子生物学
  • 生物化学

背景情况:

  • 心肌细胞克里普尔样因子 (KLF) 5 调节心脏脂肪酸的氧化.
  • 心力衰竭与脂肪酸氧化发生变化有关.

研究的目的:

  • 研究心肌细胞KLF5在脂质代谢中的作用.
  • 确定KLF5在缺血性心力衰竭的病理生理学的作用.

主要方法:

  • 在人类和小鼠缺血性心力衰竭模型中评估KLF5表达.
  • 在小鼠中利用KLF5抑制 (ML264,KLF5删除) 和过度表达 (αMHC- KLF5).
  • 通过LC-MS,西斑和qPCR分析了脂质代谢和胺路径.
  • 通过二维心声学评估心脏功能.

主要成果:

  • 在人类和小鼠缺血性心力衰竭中增加KLF5表达.
  • 在心脏病发作后,KLF5抑制改善了喷射分数和心室体积和心脏重量.
  • 通过抑制SPTLC1/ 2表达,KLF5切除降低了心肌胺水平.
  • 过度表达KLF5增加了胺,导致心功能障碍,而这种功能障碍则被氨酸治疗.

结论:

  • 在缺血性心力衰竭中诱导KLF5,并刺激胺生物合成.
  • 在患有心脏病的小鼠中抑制KLF5可以防止胺的积累,并改善心脏功能.
  • KLF5代表了缺血性心力衰竭的新疗法目标.