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Article

Inhibition of p66ShcA redox activity in cardiac muscle cells attenuates hyperglycemia-induced oxidative stress and apoptosis.

American journal of physiology. Heart and circulatory physiology - 1 Feb 2009

Malhotra Ashwani, Vashistha Himanshu, Yadav Virendra S, Dube Michael G, Kalra Satya P, Abdellatif Maha, Meggs Leonard G

Abstract excerpt

Apoptotic myocyte cell death, diastolic dysfunction, and progressive deterioration in left ventricular pump function characterize the clinical course of diabetic cardiomyopathy. A key question concerns the mechanism(s) by which hyperglycemia (HG) transmits danger signals in cardiac muscle cells. The growth factor adapter protein p66ShcA is a genetic determinant of longevity, which controls mitochondrial...

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Source

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Identifiers

PMID: 19060130
DOI: 10.1152/ajpheart.00225.2008
PMCID: PMC2643882

Provenance

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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Click a neighbor to travelStep 1 · 12 closest

Inhibition of p66ShcA redox activity in cardiac muscle cells attenuates hyperglycemia-induced oxidative stress and apoptosis.PMID 19060130Read ↗

Inhibition of wild-type p66ShcA in mesangial cells prevents glycooxidant-dependent FOXO3a regulation and promotes the survival phenotype.Semantic proximity Read ↗

Protein kinase C beta and prolyl isomerase 1 regulate mitochondrial effects of the life-span determinant p66Shc.Semantic proximity Read ↗

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

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

AGE-receptor-1 counteracts cellular oxidant stress induced by AGEs via negative regulation of p66shc-dependent FKHRL1 phosphorylation.Semantic proximity Read ↗

Redox-Resistant SERCA [Sarco(endo)plasmic Reticulum Calcium ATPase] Attenuates Oxidant-Stimulated Mitochondrial Calcium and Apoptosis in Cardiac Myocytes and Pressure Overload-Induced Myocardial Failure in Mice.Semantic proximity Read ↗

Inhibition of p66ShcA longevity gene rescues podocytes from HIV-1-induced oxidative stress and apoptosis.Semantic proximity Read ↗

cJun N-terminal kinase (JNK) phosphorylation of serine 36 is critical for p66Shc activation.Semantic proximity Read ↗

Oxidative stress-dependent p66Shc phosphorylation in skin fibroblasts of children with mitochondrial disorders.Semantic proximity Read ↗

Aging phenotype(s) in kidneys of diabetic mice are p66ShcA dependent.Semantic proximity Read ↗

p66SHC Promotes Apoptosis and Antagonizes Mitogenic Signaling in T CellsSemantic proximity Read ↗

P66Shc signals to age.Semantic proximity Read ↗

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