Background: The p66(shc) protein has been shown to control cellular responses to oxidative stress, being involved in atherosclerosis in animal models. However, the relationship between the p66(shc) gene expression levels and coronary artery disease (CAD) in humans remains unknown. In this study, we examined whether the p66(shc) gene expression in peripheral blood monocytes (PBMs) was increased in patients with CAD, compared with age- and sex-matched subjects without CAD.
Hypothesis: We hypothesize that the p66(shc) gene expression level in PBMs is increased in patients with CAD.
Methods: Forty consecutive Japanese subjects who underwent coronary angiography for suspected CAD were enrolled in this study. The p66(shc) gene expression levels in PBMs were quantitatively measured by real-time reverse transcription-polymerase chain reactions. Uni- and multivariate analyses were applied for the correlates of CAD. CAD was diagnosed if there was > 75% obstruction of at least 1 major coronary artery or a history of percutaneous coronary intervention.
Results: There were no significant differences of blood chemistries and clinical characteristics between the patients with and without CAD, except the number of subjects who were on hypertension medication. The p66(shc) gene expression levels in PBMs were significantly higher in CAD patients compared with non-CAD subjects. Multiple stepwise regression analysis revealed that the p66(shc) gene expression levels and hypertension medication were independently related to CAD (R(2)=0.287). Further, the p66(shc) gene expres- sion levels were significantly increased (P < 0.05) in proportion to the number of diseased vessels.
Conclusions: The present study is the first demonstration that increased the p66(shc) gene expression in PBMs is independently associated with CAD in Japanese subjects. The p66(shc) gene expression level in PBMs may be a novel biomarker of CAD in humans.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6653518 | PMC |
| http://dx.doi.org/10.1002/clc.20761 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
p66shc deficiency attenuates high glucose-induced autophagy dysfunction in Schwann cells.
Korean J Physiol Pharmacol
January 2025
Department of Physiology & Medical Science, College of Medicine, Chungnam National University, Daejeon 34134, Korea.
Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN.
View Article and Find Full Text PDFThe mitochondria-related gene risk mode revealed p66Shc as a prognostic mitochondria-related gene of glioblastoma.
Sci Rep
May 2024
Department of Neurosurgery, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, 410008, Hunan, People's Republic of China.
Numerous studies have highlighted the pivotal role of mitochondria-related genes (MRGs) in the initiation and progression of glioblastoma (GBM). However, the specific contributions of MRGs coding proteins to GBM pathology remain incompletely elucidated. The identification of prognostic MRGs in GBM holds promise for the development of personalized targeted therapies and the enhancement of patient prognosis.
View Article and Find Full Text PDFHigh glucose-induced p66Shc mitochondrial translocation regulates autophagy initiation and autophagosome formation in syncytiotrophoblast and extravillous trophoblast.
Cell Commun Signal
April 2024
Department of Histology and Embryology, TaiKang Medical School (School of Basic Medical Sciences), Wuhan University, Hubei Province, Wuhan, 430071, China.
Background: p66Shc, as a redox enzyme, regulates reactive oxygen species (ROS) production in mitochondria and autophagy. However, the mechanisms by which p66Shc affects autophagosome formation are not fully understood.
Methods: p66Shc expression and its location in the trophoblast cells were detected in vivo and in vitro.
DNA hypomethylation of Syk induces oxidative stress and apoptosis via the PKCβ/P66shc signaling pathway in diabetic kidney disease.
FASEB J
March 2024
Division of Nephrology, West China Hospital of Sichuan University, Chengdu, Sichuan, China.
Epigenetic alterations, especially DNA methylation, have been shown to play a role in the pathogenesis of diabetes mellitus (DM) and its complications, including diabetic kidney disease (DKD). Spleen tyrosine kinase (Syk) is known to be involved in immune and inflammatory disorders. We, therefore, investigated the possible involvement of Syk promoter methylation in DKD, and the mechanisms underlying this process.
View Article and Find Full Text PDFThe p66 Redox Protein and the Emerging Complications of Diabetes.
Int J Mol Sci
December 2023
Department of Precision and Regenerative Medicine and Ionian Area, Section of Internal Medicine, Endocrinology, Andrology and Metabolic Diseases, University of Bari Aldo Moro, 70124 Bari, Italy.
Diabetes mellitus is a chronic metabolic disease, the prevalence of which is constantly increasing worldwide. It is often burdened by disabling comorbidities that reduce the quality and expectancy of life of the affected individuals. The traditional complications of diabetes are generally described as macrovascular complications (e.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!