Jove
Visualize
お問い合わせ
JoVE
x logofacebook logolinkedin logoyoutube logo
JoVEについて
概要リーダーシップブログJoVEヘルプセンター
著者向け
出版プロセス編集委員会範囲と方針査読よくある質問投稿
図書館員向け
推薦の声購読アクセスリソース図書館諮問委員会よくある質問
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experimentsアーカイブ
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教員リソースセンター教員サイト
利用規約
プライバシーポリシー
ポリシー

関連する概念動画

Myocarditis I: Introduction01:21

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...
Myocarditis III: Medical Management01:14

Myocarditis III: Medical Management

Myocarditis: Comprehensive Medical ManagementMyocarditis, the heart muscle inflammation, requires a comprehensive medical management strategy that addresses the underlying cause, provides supportive care, manages symptoms, and reduces cardiac workload.Infections and Autoimmune CausesAdminister appropriate antimicrobial therapy when an infectious agent causes myocarditis. For instance, penicillin treats infections caused by Group A Streptococcus. In cases where autoimmune processes are...
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,...
Acute Coronary Syndrome IV: Interprofessional Care01:28

Acute Coronary Syndrome IV: Interprofessional Care

IntroductionThe management of Acute Coronary Syndrome (ACS) aims to minimize myocardial damage, preserve myocardial function, and prevent complications.Initial ManagementInpatient management involves continuous cardiac monitoring, preferably in an ICU, focusing on blood pressure, serum sodium, potassium, and creatinine levels, and urine output. Ongoing pharmacologic management is crucial for stabilizing the patient.Supplemental Oxygen: Administer supplemental oxygen if oxygen saturation is...
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...

こちらも読む

関連記事

共著者、ジャーナル、引用グラフによってこの研究に関連する記事。

並び替え
Same author

A 3D-printed extravascular stent containing sirtuin-3 engineered human bone marrow mesenchymal stem cells maintains venous graft patency.

Stem cell research & therapy·2026
Same author

CASPR2 antibody-related neurological syndromes in children: three cases report and literature review.

BMC pediatrics·2026
Same author

B cells drive CD4 T cell immunosenescence and age-associated health decline.

Science immunology·2026
Same author

Impaired autophagy flux contributes to enhanced ischemia reperfusion injury in the diabetic heart.

Autophagy reports·2025
Same author

A Novel Protein NAB1-356 Encoded by circRNA circNAB1 Mitigates Atrial Fibrillation by Reducing Inflammation and Fibrosis.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2025
Same author

A conductive polymer restores connexin43 expression through the suppression of mitogen-activated protein kinases to improve intercellular communication and alleviate atrial fibrillation.

Acta biomaterialia·2025

関連する実験動画

Updated: Jul 11, 2026

Myocardial Infarction and Functional Outcome Assessment in Pigs
12:03

Myocardial Infarction and Functional Outcome Assessment in Pigs

Published on: April 25, 2014

c-kit機能障害は,心臓発作後の心筋梗塞の治癒を阻害する.

Massimo Cimini1, Shafie Fazel, Sun Zhuo

  • 1Division of Cardiovascular Surgery, Toronto General Hospital, University Health Network, University of Toronto, Ontario, Canada.

Circulation
|September 14, 2007
PubMed
まとめ

骨髄のc-kit受容体の機能は,心筋梗塞 (MI) の後の心臓の修復に不可欠です. c-kit+細胞の浸透を促進すると,心臓の治癒が改善され,心臓発作の拡大が減少する可能性があります.

さらに関連する動画

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
07:50

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model

Published on: September 3, 2020

LAD-Ligation: A Murine Model of Myocardial Infarction
08:23

LAD-Ligation: A Murine Model of Myocardial Infarction

Published on: October 14, 2009

関連する実験動画

Last Updated: Jul 11, 2026

Myocardial Infarction and Functional Outcome Assessment in Pigs
12:03

Myocardial Infarction and Functional Outcome Assessment in Pigs

Published on: April 25, 2014

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
07:50

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model

Published on: September 3, 2020

LAD-Ligation: A Murine Model of Myocardial Infarction
08:23

LAD-Ligation: A Murine Model of Myocardial Infarction

Published on: October 14, 2009

科学分野:

  • 心血管生物学 心血管生物学
  • 血液学 ヘマトロジ
  • 再生医学は,再生医療である.

背景:

  • 骨髄幹細胞におけるc-kit受容体機能の役割は,心臓修復におけるその可能性のために調査されています.
  • 心筋梗塞 (MI) は骨髄由来細胞が重要な役割を果たす複雑な治癒プロセスを引き起こす.

研究 の 目的:

  • 骨髄におけるc-kit受容体機能が,心筋梗塞 (MI) の後の心筋の再構築と修復における重要性を評価する.
  • c-kit+細胞が心筋梗塞の拡張,血管化,および心筋線維芽細胞の反応に及ぼす影響を調査する.

主な方法:

  • 利用キット (W) /キット (W-v) c-キット変異マウスと野生型の littermates を使用して,冠動脈結束後の心臓リモデリングを研究しました.
  • 顕微鏡検査とフローサイトメトリーを用いて心室の膨張,心臓発作の膨張,滑らかな筋肉のアルファアクチン発現細胞,CD31発現血管を評価した.
  • 機能的なc-kit+細胞の救済効果を評価するために,野生型から突然変異したマウスに骨髄移植を行いました.

主要な成果:

  • 機能的なc-kitが欠けていた突然変異のマウスは,野生型対照と比較して,かなり大きな心房の膨張と心臓発作の膨張を示した.
  • ミュータントマウスでは,アルファアクチン発現細胞とCD31発現血管の増殖および総滑らかな筋肉の有意な減少が観察されました.
  • 骨髄移植は,突然変異したマウスの血管化とミオフィブロブラスト集団を回復させ,心臓発作の拡大を減少させた.

結論:

  • 骨髄のc-kit機能は,心臓梗塞におけるミオフィブロブラストの修復反応に不可欠である.
  • c-kit+細胞の浸透を増加させることを目的とした介入は,内生的な修復を強化し,心臓発作の拡大を予防し,心臓発作後の心臓機能を改善することを約束しています.