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PAR2 Regulates Cardiac Pressure and Vascular Function Through Context-Dependent Signalling Mechanisms
Joselia Carlos1,2, Filip Konecny1,3,4, Maryia Ryskina1
1Department of Medical Biophysics, Schulich School of Medicine and Dentistry, Western University, London, ON N6A 5C1, Canada.
Current Issues in Molecular Biology
|July 28, 2026
Summary
Proteinase-activated receptor-2 (PAR2) deficiency causes high blood pressure but maintains heart function. PAR2 activation lowers cardiac pressure but affects vascular responses differently in PAR2-deficient mice.
Area of Science:
- Cardiovascular Physiology
- G Protein-Coupled Receptor Signaling
Background:
- Proteinase-activated receptor-2 (PAR2) influences cardiac pressure and vascular tone via complex signaling pathways.
- Understanding PAR2's role is crucial for cardiovascular health.
Purpose of the Study:
- To investigate the baseline cardiovascular phenotype of PAR2-deficient (PAR2-/-) mice.
- To examine the in vivo effects of the PAR2 agonist tcLIGRLO on cardiovascular function.
Main Methods:
- Left ventricular pressure-volume (PV) analysis in PAR2-/- and wild-type (WT) mice.
- In vivo administration of the PAR2 agonist tcLIGRLO.
- Ex vivo assessment of vascular responses in PAR2-/- arteries.
Main Results:
- PAR2-/- mice exhibited elevated systolic and diastolic pressures with preserved global cardiac function.
- tcLIGRLO reduced cardiac pressure and contractility in WT mice, but not in PAR2-/- mice.
- tcLIGRLO induced strain-dependent vascular responses in PAR2-/- mice, involving Gq-dependent signaling.
Conclusions:
- PAR2 acts as a context-dependent regulator of cardiac pressure and vascular tone.
- PAR2-dependent cardiac regulation and PAR2-independent vascular responses involve distinct signaling mechanisms.
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