Publications by authors named "G Vial"

This study evaluates the safety and potential benefits of PBM on pancreatic beta cells and islets. PBM was applied to insulin-secreting cell lines (MIN6) and rat pancreatic islets using a 670 nm light source, continuous output, with a power density of 2.8 mW/cm², from 5 s to several 24 h.

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Article Synopsis
  • Obstructive sleep apnea (OSA) impacts nearly 1 billion people globally, causing chronic intermittent hypoxia (CIH) that leads to organ damage, especially affecting the heart and visceral white adipose tissue (WAT).
  • The study aimed to explore if CIH causes premature senescence in visceral WAT, which in turn may trigger changes in heart structure and function.
  • Results showed that CIH caused significant changes in WAT and early signs of heart damage, but these effects could be mitigated through surgical removal of fat tissue or deletion of specific genes, highlighting visceral WAT senescence as a promising target for combating OSA-related issues.
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Obstructive sleep apnea (OSA) induces intermittent hypoxia (IH), an independent risk factor for non-alcoholic fatty liver disease (NAFLD). While the molecular links between IH and NAFLD progression are unclear, immune cell-driven inflammation plays a crucial role in NAFLD pathogenesis. Using lean mice exposed to long-term IH and a cohort of lean OSA patients (n = 71), we conducted comprehensive hepatic transcriptomics, lipidomics, and targeted serum proteomics.

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Elastic fibers, made of elastin (90%) and fibrillin-rich microfibrils (10%), are the key extracellular components, which endow the arteries with elasticity. The alteration of elastic fibers leads to cardiovascular dysfunctions, as observed in elastin haploinsufficiency in mice () or humans (supravalvular aortic stenosis or Williams-Beuren syndrome). In and mice, we evaluated (arteriography, histology, qPCR, Western blots and cell cultures) the beneficial impact of treatment with a synthetic elastic protein (SEP), mimicking several domains of tropoelastin, the precursor of elastin, including hydrophobic elasticity-related domains and binding sites for elastin receptors.

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