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Cristina López-Vicario

Researcher at University of Barcelona

Publications -  49
Citations -  7780

Cristina López-Vicario is an academic researcher from University of Barcelona. The author has contributed to research in topics: Inflammation & Adipose tissue. The author has an hindex of 23, co-authored 41 publications receiving 6700 citations.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Resolvin D1 and Its Precursor Docosahexaenoic Acid Promote Resolution of Adipose Tissue Inflammation by Eliciting Macrophage Polarization toward an M2-Like Phenotype

TL;DR: Novel mechanisms underlying ω-3-polyunsaturated fatty acid actions on adipose tissue, adipocytes, and stromal vascular cells (SVC) are reported and resolvin D1 and its precursor DHA confer anti-inflammatory and proresolving actions in inflamed adiposes tissue.
Journal ArticleDOI

Role for PPARγ in obesity-induced hepatic steatosis as determined by hepatocyte- and macrophage-specific conditional knockouts

TL;DR: Findings establish PPARγ expression in hepatocytes as a prosteatotic factor in fatty liver disease as determined by hepatocyte‐ and macrophage‐specific conditional knockouts.
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Molecular interplay between Δ5/Δ6 desaturases and long-chain fatty acids in the pathogenesis of non-alcoholic steatohepatitis

TL;DR: Investigating gene expression profiling of liver biopsies from NASH patients with translational studies in mouse models of steatohepatitis and pharmacological interventions in isolated hepatocytes to identify new molecular targets in NASH indicates that impaired hepatic fatty acid desaturation and unbalanced ω-6 to ψ-3 ratio play a role in the pathogenesis of NASH.