Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Oxidative stress in cardiovascular diseases and obesity: role of p66Shc and protein kinase C

De Marchi E., Baldassari F., Bononi A., Wieckowski MR., Pinton P.

Narrative Review, published in Oxid Med Cell Longev (2013) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Oxid Med Cell Longev (2013)
Reported sample size
—
Source database
Europe PMC
PMID
23606925
PMCID
PMC3625561
DOI
10.1155/2013/564961
Citations
92

Abstract (original English)

Reactive oxygen species (ROS) are a byproduct of the normal metabolism of oxygen and have important roles in cell signalling and homeostasis. An imbalance between ROS production and the cellular antioxidant defence system leads to oxidative stress. Environmental factors and genetic interactions play key roles in oxidative stress mediated pathologies. In this paper, we focus on cardiovascular diseases and obesity, disorders strongly related to each other; in which oxidative stress plays a fundamental role. We provide evidence of the key role played by p66(Shc) protein and protein kinase C (PKC) in these pathologies by their intracellular regulation of redox balance and oxidative stress levels. Additionally, we discuss possible therapeutic strategies aimed at attenuating the oxidative damage in these diseases.

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AdipocytesHumansCardiovascular DiseasesObesityReactive Oxygen SpeciesProtein Kinase CCell DifferentiationOxidative StressShc Signaling Adaptor ProteinsSrc Homology 2 Domain-Containing, Transforming Protein 1

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