Loss of atrioventricular conduction system (AVCS) cells due to either inherited or acquired deficits leads to conduction diseases, which can deteriorate into fatal cardiac arrhythmias and sudden death. In this issue of the JCI, Wang et al. constructed a mouse model of atrioventricular block (AVB) by inducing AVCS cell-specific injury using the Cx30.2 enhancer to drive expression of diphtheria toxin fragment A. AVCS cell ablation in adult mice led to irreversible AVB. jkjkIn contrast, AVCS cell injury in neonatal mice was followed by spontaneous recovery in a subset of mice, revealing a limited postnatal time window during which the regeneration of AVCS cells can occur as a result of cellular plasticity. This exciting study paves the way for future research into biological or cellular treatment approaches for cardiac conduction diseases by exploiting the regenerative potential of AVCS cells.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8483745PMC
http://dx.doi.org/10.1172/JCI152185DOI Listing

Publication Analysis

Top Keywords

avcs cells
12
cardiac conduction
8
conduction diseases
8
avcs cell
8
avcs
6
cellular regeneration
4
regeneration potential
4
potential strategy
4
strategy treat
4
treat cardiac
4

Similar Publications

Article Synopsis
  • The study investigated the link between epicardial adipose tissue (EAT) characteristics and aortic valve calcification (AVC) using CT scans in 43 patients before heart surgery.
  • Results showed that EAT density was positively correlated with the quantity of inflammatory macrophages and osteocalcin-positive cells, indicating a relationship between inflammation in EAT and AVC severity.
  • The findings suggest that higher EAT density, along with certain immune cell counts, may indicate more severe aortic valve degeneration, highlighting the importance of EAT in cardiovascular health.
View Article and Find Full Text PDF

The cardiac conduction system (CCS) ensures regular contractile function, and injury to any of its components can cause cardiac dysrhythmia. Although all cardiomyocytes (CMs) originate from common progenitors, the CCS is composed of biologically distinct cell types with unique functional and developmental characteristics. In contrast to ventricular cardiomyocytes, which continue to proliferate after birth, most CCS cells terminally exit the cell cycle during fetal development.

View Article and Find Full Text PDF

Loss of atrioventricular conduction system (AVCS) cells due to either inherited or acquired deficits leads to conduction diseases, which can deteriorate into fatal cardiac arrhythmias and sudden death. In this issue of the JCI, Wang et al. constructed a mouse model of atrioventricular block (AVB) by inducing AVCS cell-specific injury using the Cx30.

View Article and Find Full Text PDF

During development, the ventricles of mammals and birds acquire a specialized pattern of electrical activation with the formation of the atrioventricular conduction system (AVCS), which coincides with the completion of ventricular septation. We investigated whether AVCS formation coincides with ventricular septation in developing Siamese crocodiles (). Comparisons were made with Amazon toadhead turtle () with a partial septum only and no AVCS (negative control) and with chicken () (septum and AVCS, positive control).

View Article and Find Full Text PDF

Novel hemodynamic structures in the human glomerulus.

Am J Physiol Renal Physiol

November 2018

Bristol Renal and School of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol , United Kingdom.

To investigate human glomerular structure under conditions of physiological perfusion, we have analyzed fresh and perfusion-fixed normal human glomeruli at physiological hydrostatic and oncotic pressures using serial resin section reconstruction, confocal, multiphoton, and electron microscope imaging. Afferent and efferent arterioles (21.5 ± 1.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!