Key result
High afterload alone induced a 50% increase in c-myc (95% CI 32-72%) and 54% increase in c-fos (95% CI 27-86%), and a 32% suppression of H-ras (95% CI 25-40%) in isolated working rat hearts.
Effect estimate: 50% increase of c-myc (95% CI 32-72)
p-value: p=<0.0001
Increased pressure alone, without circulating angiotensin II, can induce proto-oncogene expression similar to that seen in the hypertrophying heart.
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Should not alter clinical practice; leaves open whether afterload-driven gene changes contribute to human hypertrophy.
Roffe et al. (1996) studied Experimental hypertension model (isolated working rat heart). High afterload (140 mmHg) with or without angiotensin II vs. Low afterload (60 mmHg) with or without angiotensin II was evaluated on Proto-oncogene mRNA induction (c-myc, c-fos, H-ras) in the left ventricle (50% increase of c-myc, 95% CI 32-72, p=<0.0001). High afterload alone induced a 50% increase in c-myc (95% CI 32-72%) and 54% increase in c-fos (95% CI 27-86%), and a 32% suppression of H-ras (95% CI 25-40%) in isolated working rat hearts.
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