Focal adhesion kinase and endothelial cell apoptosis

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Updated: Jun 1, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Qing Lu1, Sharon Rounds

  • 1Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA.

Microvascular Research
|June 1, 2011
PubMed

Insights

Focal adhesion kinase (FAK) is crucial for cell survival and adhesion. This review details FAK signaling pathways that prevent apoptosis and its role in cardiovascular diseases.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Focal adhesion kinase (FAK) is integral to focal adhesion complexes, mediating cell-substratum adhesion.
  • FAK signaling disruption leads to anoikis (apoptosis) in anchorage-dependent cells, including endothelial cells.
  • Basal FAK activity, regulated by PI3K/Akt and small GTPases, maintains endothelial cell adhesion.

Purpose of the Study:

  • To review FAK signaling pathways involved in preventing apoptosis.
  • To elucidate FAK's role in adenosine and homocysteine-induced endothelial cell apoptosis.
  • To explore FAK's significance in cardiovascular diseases.

Main Methods:

  • Literature review of FAK signaling pathways.
  • Analysis of FAK's role in cellular apoptosis.
  • Examination of FAK's involvement in cardiovascular pathologies.

Main Results:

  • FAK is essential for normal cell survival and substrate adhesion.
  • FAK activity is regulated by PI3K/Akt and small GTPase signaling.
  • FAK plays a role in cardiomyocyte hypertrophy and hypoxia/reoxygenation-induced cell death.

Conclusions:

  • FAK signaling is a key mechanism for preventing apoptosis in endothelial cells.
  • Dysregulation of FAK contributes to endothelial cell apoptosis and cardiovascular diseases.
  • Targeting FAK pathways may offer therapeutic strategies for cardiovascular conditions.

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