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Related Concept Videos

Intracellular Signaling Affects Focal Adhesions01:17

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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.
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The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last...
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The adherens junctions that anchor cells together are multi-protein complexes that dynamically adapt to mechanical stimuli such as tensile forces and shear stress. Mechanosensory proteins in these junctions can sense such mechanical stimuli and undergo a shift in their conformation, resulting in an altered function — a process called mechanotransduction.
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Related Experiment Video

Updated: May 16, 2025

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
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Calpain-2-Mediated Endothelial Focal Adhesion Disruption in Thoracic Aortic Dissection.

Xiaomei Teng1,2, Yansong Wang2, Haoyue Huang1,2

  • 1Department of Cardiovascular Surgery of the First Affiliated Hospital of Soochow University, 899 Pinghai Road, Suzhou, 215006, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|April 2, 2025
PubMed
Summary

Calpain-2 dysregulation drives thoracic aortic dissection (TAD) by damaging endothelial cells. Inhibiting calpain shows promise for preventing and treating this life-threatening condition.

Keywords:
Calpain‐2ItgavTalinfocal adhesionthoracic aortic dissection

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Pathology

Background:

  • Thoracic aortic dissection (TAD) is a critical condition with high mortality.
  • Early-stage TAD is linked to endothelial barrier dysfunction, but mechanisms are unclear.

Purpose of the Study:

  • Investigate the role of Calpain-2 in early TAD pathogenesis.
  • Identify therapeutic targets for TAD prevention and treatment.

Main Methods:

  • Single-cell RNA sequencing on patient data.
  • Murine models of TAD induced by β-aminopropionitrile (BAPN).
  • Endothelial-specific and macrophage-specific Capns1 knockout models.

Main Results:

  • Dysregulated Calpain-2 expression affects endothelial focal adhesion proteins in early TAD.
  • Elevated plasma calpain activity correlates with TAD risk and organ dysfunction.
  • Calpain inhibition prevents TAD in murine models.
  • Endothelial-specific Capns1 deletion reduces TAD incidence by preserving focal adhesion integrity.
  • Macrophage Capns1 deletion accelerates rupture in later stages.
  • Angiotensin II upregulates Calpain-2, compromising endothelial integrity.

Conclusions:

  • Calpain-2 is an early pathological hallmark and driver of TAD.
  • Targeting calpain offers a potential therapeutic strategy for TAD.