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Article

Genetic deletion of the p66Shc adaptor protein protects from angiotensin II-induced myocardial damage.

Hypertension (Dallas, Tex. : 1979) - 1 Aug 2005

Graiani Gallia, Lagrasta Costanza, Migliaccio Enrica, Spillmann Frank, Meloni Marco, Madeddu Paolo, Quaini Federico, Padura Ines Martin, Lanfrancone Luisa, Pelicci PierGiuseppe, Emanueli Costanza

Abstract excerpt

Angiotensin II (Ang II), acting through its G protein-coupled AT1 receptor (AT1), contributes to the precocious heart senescence typical of patients with hypertension, atherosclerosis, and diabetes. AT1 was suggested to transactivate an intracellular signaling controlled by growth factors and their tyrosin-kinase receptors. In cultured vascular smooth muscle cells, this downstream mechanism comprises the p66Shc...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 15998704
DOI: 10.1161/01.HYP.0000174986.73346.ba

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Genetic deletion of the p66Shc adaptor protein protects from angiotensin II-induced myocardial damage.PMID 15998704Read ↗

Diabetes Promotes Cardiac Stem Cell Aging and Heart Failure, Which Are Prevented by Deletion of the p66 <sup>shc</sup> GeneSemantic proximity Read ↗

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p66Shc deletion confers vascular protection in advanced atherosclerosis in hypercholesterolemic apolipoprotein E knockout mice.Semantic proximity Read ↗

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