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Related Concept Videos

Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Adherens Junctions01:24

Adherens Junctions

Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
Adherens Junctions are Dynamic
The endothelial cells...
Anchoring Junctions01:03

Anchoring Junctions

Anchoring junctions are multiprotein complexes that help cells connect to other cells and the extracellular matrix. Anchoring junctions are present on the lateral and basal surfaces of cells, providing strong and flexible connections. Focal adhesions are often formed due to cell interactions with the ECM substrata, which initiate signal transduction via kinase cascades and other mechanisms. Together, they provide stability and tissue integrity. There are three types of anchoring junctions:...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
Desmosomes01:05

Desmosomes

The term desmosome derives from the Greek words "desmo" and "soma" meaning "adhesion bodies." This structure was first observed during the late 1800s and described as small, dense nodules in the epidermis. Desmosomes are button-like structures that help form an interlinked network of intermediate filaments across the cells. These junctions are  essential to hold cells together under mechanical stress and to maintain tissue integrity. Desmosomes are multi-protein complexes comprising desmosomal...

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Related Experiment Video

Updated: Jul 8, 2026

Optimizing Attachment of Human Mesenchymal Stem Cells on Poly(ε-caprolactone) Electrospun Yarns
10:50

Optimizing Attachment of Human Mesenchymal Stem Cells on Poly(ε-caprolactone) Electrospun Yarns

Published on: April 10, 2015

Adhesion proteins, stem cells, and arrhythmogenesis.

Nikki Gillum1, Narine Sarvazyan

  • 1Pharmacology and Physiology Department, The George Washington University, 2300 Eye Street, Washington, DC 20037, USA.

Cardiovascular Toxicology
|January 8, 2008
PubMed
Summary
This summary is machine-generated.

Cell-transplantation therapy aims to repair heart muscle by improving cell engraftment. Enhancing cell adhesion may improve cardiac repair and reduce arrhythmia risk.

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Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity
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Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity

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Generation of Aligned Functional Myocardial Tissue Through Microcontact Printing
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Generation of Aligned Functional Myocardial Tissue Through Microcontact Printing

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Last Updated: Jul 8, 2026

Optimizing Attachment of Human Mesenchymal Stem Cells on Poly(ε-caprolactone) Electrospun Yarns
10:50

Optimizing Attachment of Human Mesenchymal Stem Cells on Poly(ε-caprolactone) Electrospun Yarns

Published on: April 10, 2015

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity
08:00

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity

Published on: July 10, 2019

Generation of Aligned Functional Myocardial Tissue Through Microcontact Printing
11:09

Generation of Aligned Functional Myocardial Tissue Through Microcontact Printing

Published on: March 19, 2013

Area of Science:

  • Cardiovascular Research
  • Regenerative Medicine
  • Cardiac Electrophysiology

Background:

  • Cell-transplantation therapy shows promise for cardiac repair.
  • Key goals include restoring cardiac architecture and electrical function while preventing adverse effects like hypertrophy and scarring.
  • Successful engraftment of transplanted cells is crucial for therapeutic efficacy.

Purpose of the Study:

  • To review recent advancements in cell-transplantation therapy for cardiac repair.
  • To highlight challenges in confirming and functionally characterizing cell engraftment.
  • To discuss strategies for improving cell engraftment and mitigating associated risks.

Main Methods:

  • Review of current literature on cell-transplantation for cardiac repair.
  • Analysis of challenges in assessing cell engraftment and function.
  • Exploration of cell adhesion modulation as a therapeutic strategy.

Main Results:

  • Incomplete or partial cell engraftment can worsen myocardial heterogeneity and increase arrhythmia susceptibility.
  • Confirmation and functional characterization of engrafted cells remain significant hurdles.
  • Modulating cell adhesion through coupling proteins presents a potential solution.

Conclusions:

  • Effective cell engraftment is critical for successful cardiac repair via transplantation.
  • Addressing engraftment challenges is essential to prevent adverse outcomes like arrhythmias.
  • Targeting cell adhesion mechanisms offers a promising avenue to enhance cardiac graft integration and function.