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Development of the Heart

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...

Heart Failure II: Pathophysiology

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...

Cardiomyopathy II: Dilated Cardiomyopathy

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,...

Pathophysiology of Heart Failure

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...

Pathophysiology of Cardiac Performance

Pathophysiology of Cardiac Performance

Typical heart performance is influenced by heart rate, rhythm, myocardial contraction, and metabolism or blood flow. The cardiac muscle exhibits distinct electrophysiological features, including pacemaker activity and calcium channel control, which play a vital role in the heart's response to various drugs. The autonomic nervous system, comprising the sympathetic and parasympathetic branches, regulates heart rate. Sympathetic activation increases heart rate, while parasympathetic activation...

Heart Failure I: Introduction

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...

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Related Experiment Video

Updated: Apr 26, 2026

Capturing the Cardiac Injury Response of Targeted Cell Populations via Cleared Heart Three-Dimensional Imaging

Capturing the Cardiac Injury Response of Targeted Cell Populations via Cleared Heart Three-Dimensional Imaging

Published on: March 17, 2020

Rejuvenating the damaged and aged heart: lessons from development.

Ge Liu¹, Hanchao Gao¹, Xinyu Liu²

¹Department of Geriatric Medicine, Shenzhen Longhua District Central Hospital, Shenzhen, China.

Npj Biomedical Innovations

|April 24, 2026

Summary

This summary is machine-generated.

Mammals lose heart regeneration for strong contractions. Reactivating juvenile cell growth pathways may restore cardiac repair in aging hearts.

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Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration

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

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

Published on: June 3, 2018

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Last Updated: Apr 26, 2026

Capturing the Cardiac Injury Response of Targeted Cell Populations via Cleared Heart Three-Dimensional Imaging

Capturing the Cardiac Injury Response of Targeted Cell Populations via Cleared Heart Three-Dimensional Imaging

Published on: March 17, 2020

Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration

Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration

Published on: May 24, 2016

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

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

Published on: June 3, 2018

Area of Science:

Cardiovascular Biology
Developmental Biology
Regenerative Medicine

Background:

Mammals exhibit limited cardiac regeneration due to an evolutionary trade-off for high-output contractile function.
Cardiomyocyte cell-cycle withdrawal is regulated by metabolic, epigenetic, and microenvironmental factors during development.

Purpose of the Study:

To explore strategies for restoring cardiomyocyte proliferative potential in adult mammals.
To investigate the potential of reprogramming juvenile regulatory networks to enhance cardiac regeneration.

Main Methods:

Induction of specific transcription factors.
Metabolic reprogramming of cardiomyocytes.
Modulation of the cardiac cellular niche.

Main Results:

Juvenile regulatory networks hold potential for restoring proliferative capacity in adult cardiomyocytes.
Cardiac aging mirrors developmental disruptions in regenerative mechanisms.

Conclusions:

Reprogramming strategies targeting developmental barriers may counteract cardiac senescence.
Restoring regenerative potential is a promising therapeutic avenue for aging hearts.