Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

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...

Regulation of Heart Rates

Regulation of Heart Rates

The regulation of heart rate is a complex process controlled by the autonomic nervous system (ANS), hormonal influences, and intrinsic cardiac mechanisms. The ANS has two main components: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS).
The SNS increases heart rate through the release of norepinephrine and epinephrine, which act on beta-1 adrenergic receptors in the heart. This action increases the rate of depolarization in the sinoatrial (SA) node, the heart's...

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Intergenic trans-splicing-driven formation of a chimeric FAM168B::ANKRD42 transcript in prostate cancer.

3 Biotech·2026

Same author

Aberrant activation of FAM168B via chimeric PLEKHB2::FAM168B mRNA promotes breast invasive cancer progression.

Biochemical and biophysical research communications·2026

Same author

Entomopathogenic Nematode <i>Steinernema carpocapsae</i> Venom Proteins Disrupt Developmental Physiology and Reproduction of <i>Spodoptera frugiperda</i> (Lepidoptera: Noctuidae).

Toxins·2026

Same author

Tumor exosomes impact functional hallmarks of cancer.

Cancer metastasis reviews·2026

Same author

Carotid arteries in cerebral small vessel disease and dementia.

Acta neuropathologica communications·2026

Same author

Author Correction: Enterovirus-A71 exploits peripherin and Rac1 to invade the central nervous system.

EMBO reports·2026

Search research articles

Related Experiment Video

Updated: May 26, 2026

Viral Transgene Expression in Rodent Hearts and the Assessment of Cardiac Arrhythmia Risk

Viral Transgene Expression in Rodent Hearts and the Assessment of Cardiac Arrhythmia Risk

Published on: July 27, 2022

Neuronal p60TRP expression modulates cardiac capacity.

Manisha Mishra¹, Arulmani Manavalan, Siu Kwan Sze

¹School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore 637551, Singapore.

Journal of Proteomics

|December 17, 2011

Summary

This summary is machine-generated.

Neural overexpression of p60TRP in mice significantly alters cardiac proteome, impacting cardiovascular function. This study reveals molecular insights into p60TRP

More Related Videos

Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System

Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System

Published on: May 22, 2018

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

Related Experiment Videos

Last Updated: May 26, 2026

Viral Transgene Expression in Rodent Hearts and the Assessment of Cardiac Arrhythmia Risk

Viral Transgene Expression in Rodent Hearts and the Assessment of Cardiac Arrhythmia Risk

Published on: July 27, 2022

Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System

Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System

Published on: May 22, 2018

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
Proteomics
Neuroscience

Background:

Heart failure and myocardial infarction are leading causes of global mortality.
Cardiovascular disease incidence is projected to increase worldwide.
Understanding molecular mechanisms underlying cardiac function is crucial.

Purpose of the Study:

To investigate the cardiac proteome profile in transgenic p60-Transcription Regulator Protein (p60TRP) mice.
To elucidate molecular events from long-term neural p60TRP overexpression.
To assess the implications for cardiovascular functions.

Main Methods:

Utilized an isobaric tags for relative and absolute quantitation (iTRAQ)-based proteomics approach.
Analyzed the whole heart proteome of neural transgenic p60TRP mice.
Identified and quantified protein expression levels.

Main Results:

Identified a total of 1148 proteins in the heart proteome.
Found 116 proteins significantly altered in transgenic p60TRP mouse hearts.
Observed significant changes in cardiac proteome due to neural p60TRP overexpression.

Conclusions:

In vivo neural overexpression of p60TRP impacts cardiovascular capacities.
p60TRP demonstrates potential neuroprotective therapeutic effects.
The study provides insights into p60TRP's role in cardiac molecular events.