Related Experiment Video

Updated: May 4, 2026

Assessing Cardiomyocyte Subtypes Following Transcription Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts
09:29

Assessing Cardiomyocyte Subtypes Following Transcription Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts

Published on: March 22, 2017

7.4K

Recent advances and future prospects in direct cardiac reprogramming

Yifang Xie1,2, Ben Van Handel3, Li Qian1,2

  • 1McAllister Heart Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.

Nature Cardiovascular Research
|August 28, 2024
PubMed

Insights

Direct cardiac reprogramming converts fibroblasts into cardiomyocyte-like cells (iCMs) to repair heart damage. This review covers reprogramming methods, mechanisms, and challenges for clinical use.

Area of Science:

  • Cardiovascular Research
  • Regenerative Medicine
  • Molecular Biology

Background:

  • Cardiovascular disease is a major global health issue.
  • Limited regeneration of cardiomyocytes after myocardial infarction leads to heart failure.
  • Direct cardiac reprogramming offers a potential therapeutic strategy to replace lost cardiomyocytes.

Purpose of the Study:

  • To review cardiac reprogramming cocktails for generating induced cardiomyocyte-like cells (iCMs).
  • To explore mechanistic studies on barriers and facilitators of cardiac reprogramming.
  • To discuss recent advances, including single-cell '-omics' research, and obstacles to clinical translation.

Main Methods:

  • Review of literature on cardiac reprogramming cocktails (transcription factors, microRNAs, small molecules).
  • Analysis of mechanistic studies investigating reprogramming processes.
  • Examination of single-cell '-omics' data for insights into iCM generation.

Main Results:

  • Various reprogramming cocktails effectively generate iCMs from cardiac fibroblasts.
  • Mechanistic studies reveal key factors influencing reprogramming efficiency.
  • Single-cell '-omics' technologies provide high-resolution insights into cellular transitions during reprogramming.

Conclusions:

  • Direct cardiac reprogramming is a promising strategy for treating heart failure.
  • Understanding reprogramming mechanisms and barriers is crucial for optimizing iCM generation.
  • Overcoming obstacles is essential for the clinical application of cardiac reprogramming therapies.

More Related Videos

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes09:16

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

Published on: June 3, 2018

7.3K
Assessing Cardiac Reprogramming using High Content Imaging Analysis06:02

Assessing Cardiac Reprogramming using High Content Imaging Analysis

Published on: October 26, 2020

1.3K

Related Concept Videos

Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
2.0K
Overview of the Heart01:07

Overview of the Heart

The heart, a muscular organ located in the chest, functions as the body's pump, circulating blood through the vascular system. It has four chambers: two atria on top and two ventricles below. The right atrium receives deoxygenated blood from the body and passes it to the right ventricle, which pumps it to the lungs for oxygenation. The left atrium receives oxygenated blood from the lungs and transfers it to the left ventricle, which pumps it to the rest of the body.
The heart's structure...
32.2K
Development of the Heart01:27

Development of the Heart

The development of the human heart, a crucial organ, commences from the mesoderm on the 18th or 19th day after fertilization. This process initiates in the cardiogenic area, a group of mesodermal cells at the embryo's head end, which evolves into elongated strands known as cardiogenic cords. These cords undergo a transformation to form hollow-centered endocardial tubes.
As the embryo undergoes lateral folding, these paired tubes approach each other, merging into a single primitive heart...
3.9K
Heart Failure I: Introduction01:27

Heart Failure I: Introduction

Heart failure refers to a clinical syndrome caused by structural or functional cardiac disorders that prevent the heart from pumping an adequate amount of blood to meet the body's metabolic needs. This condition often arises from myocardial infarction or ischemia, leading to decreased cardiac output, reduced tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability.Heart failure can result from disruptions in the mechanisms that regulate cardiac output...
1.7K
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...
1.9K
Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
626