July 6, 2005Hypertension

Genetic Deletion of the p66 Shc Adaptor Protein Protects From Angiotensin II–Induced Myocardial Damage

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Why the study?

Does genetic deletion of p66Shc prevent Angiotensin II-induced myocardial damage in mice?

Population

p66Shc knockout mice (p66Shc(-/-)) and wild-type littermates (p66Shc(+/+)), and isolated cardiomyocytes

Comparison

Genetic deletion of p66Shc (p66Shc) with… vs Wild-type littermates (p66Shc) with infusion of…

Design

Preclinical

Follow-up

28 days

Authors

GGGallia GraianiUniversity of Parma CLCostanza Annamaria LagrastaUniversity of Parma EMEnrica MigliaccioEuropean Institute of Oncology

Discussion

Member takes

Implication

May warrant p66Shc inhibition trials in hypertensive remodeling; leaves open translation beyond murine models.

Structured PICO

Does genetic deletion of p66Shc prevent Angiotensin II-induced myocardial damage in mice?

Population

p66Shc knockout mice (p66Shc(-/-)) and wild-type littermates (p66Shc(+/+)), and isolated cardiomyocytes

Intervention

Genetic deletion of p66Shc (p66Shc(-/-)) with infusion of sub-pressor dose of Angiotensin II (300 nmol/kg body weight daily for 28 days)

Comparator

Wild-type littermates (p66Shc(+/+)) with infusion of sub-pressor dose of Angiotensin II (300 nmol/kg body weight daily for 28 days)

Outcome

Left ventricular hypertrophy and apoptotic death of cardiomyocytes and endothelial cellssurrogate

Genetic deletion of the p66Shc adaptor protein protects the heart from Angiotensin II-induced hypertrophy and apoptosis, highlighting a potential novel therapeutic target for myocardial remodeling.

Cite This Study

Graiani et al. (2005) studied this question.

synapsesocial.com/papers/6a821cbca8461dff0846bf5d https://doi.org/10.1161/01.hyp.0000174986.73346.ba

Topics

Cardiomyopathy

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