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Mojgan Masoodi

Researcher at Nestlé

Publications -  58
Citations -  2904

Mojgan Masoodi is an academic researcher from Nestlé. The author has contributed to research in topics: Lipidomics & Lipid metabolism. The author has an hindex of 23, co-authored 51 publications receiving 2368 citations. Previous affiliations of Mojgan Masoodi include University of Cambridge & École Polytechnique Fédérale de Lausanne.

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Obesity in mice with adipocyte-specific deletion of clock component Arntl

TL;DR: A role for the adipocytes clock in the temporal organization of energy regulation is revealed, timing as a modulator of the adipocyte-hypothalamic axis is highlighted and the impact of timing of food intake on body weight is shown.
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The immunomodulatory properties of mesenchymal stem cells and their use for immunotherapy

TL;DR: Some recent literature on the mechanisms of immunomodulation by MSC in vitro and animal models are reviewed, new data on the secretion of pro-inflammatory and anti-inflammatory cytokines, chemokines and prostaglandins are presented and the hopes and expectations of MSC-based immune therapy are discussed.
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An automated shotgun lipidomics platform for high throughput, comprehensive, and quantitative analysis of blood plasma intact lipids

TL;DR: This shotgun lipidomics platform can be implemented in different laboratories without compromising reproducibility, allowing multi-site studies and inter-laboratory comparisons, and achieves absolute quantification, by inclusion of internal standards for every lipid class measured.
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Lipid signaling in adipose tissue: Connecting inflammation & metabolism

TL;DR: M2 macrophages could support remodeling of WAT to a tissue containing metabolically flexible adipocytes endowed with a high capacity of both TAG/FA cycling and oxidative phosphorylation, which enhances the formation of "healthy" adipocytes.
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The mitochondria-targeted antioxidant MitoQ decreases features of the metabolic syndrome in ATM +/-/ApoE -/- mice

TL;DR: The data suggest that MitoQ inhibits the development of multiple features of the metabolic syndrome in these mice by affecting redox signaling pathways that depend on mitochondrial ROS such as hydrogen peroxide.