Key result
Tryptase increased collagen synthesis via protease-activated receptor 2, while PAR-2 blockade with 10 μmol/L FSLLRY prevented fibrosis in spontaneously hypertensive rats.
Tryptase induces cardiac fibrosis via protease-activated receptor 2 and extracellular signal-regulated kinase signaling, highlighting a potential therapeutic target for hypertensive heart disease.
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No current role for PAR-2 blockade in hypertensive heart disease; leaves open translation from rat models to patients.
McLarty et al. (2011) studied Cardiac fibrosis in the hypertensive heart. Tryptase and PAR-2 blockade (FSLLRY) was evaluated on Collagen synthesis and fibrosis. Tryptase increased collagen synthesis via protease-activated receptor 2, while PAR-2 blockade with 10 μmol/L FSLLRY prevented fibrosis in spontaneously hypertensive rats.
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