Key result
EGFR antisense oligodeoxynucleotide reduces LV/BW ratio ~16% and lowers blood pressure in hypertensive rats.
Why the study?
To examine whether EGFR is involved in the development of left ventricular hypertrophy by inhibiting EGFR with a specific antisense oligodeoxynucleotide to attenuate Ang II-induced cardiovascular hypertrophic effects.
Does EGFR antisense oligodeoxynucleotide reduce Angiotensin II-induced cardiac hypertrophy and hypertension in rats?
Does EGFR antisense oligodeoxynucleotide reduce Angiotensin II-induced cardiac hypertrophy and hypertension in rats?
Absolute Event Rate: 2.32% vs 2.75%
p-value: p=<0.01
Inhibition of EGFR with antisense oligodeoxynucleotides attenuates Angiotensin II-induced hypertension and cardiac hypertrophy in a rat model, highlighting EGFR's role in Ang II signaling.
No takes yet. Share an insight, caveat, or question.
EGFR antagonism attenuates Ang II-induced hypertrophy and hypertension in vivo; extends VSMC transactivation findings but leaves open clinical translation.
Kagiyama et al. (2002) studied Angiotensin II-induced cardiac hypertrophy and hypertension (n=15). EGFR antisense oligodeoxynucleotide (EGFR-AS) vs. Control / EGFR-sense was evaluated on Left ventricular/body weight (LV/BW) ratio (p=<0.01). EGFR antisense oligodeoxynucleotide normalized the left ventricular/body weight ratio (2.32 vs 2.75; P<0.01) and decreased blood pressure in Angiotensin II-infused hypertensive rats.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: