Herminia González-Navarro

TL;DR: The concept of hepatic lipase as mainly a lipolytic enzyme that reduces atherogenic risk has evolved into that of a complex protein with multiple functions that, depending on genetic background and sites of expression, can have a variable effect on atherosclerosis.

TL;DR: The purpose of this review is to summarize current knowledge about the role of cell cycle regulators in the development of native and graft atherosclerosis that has arisen from animal studies, histological examination of specimens from human patients, and genetic studies.

TL;DR: It is shown that inactivating mutations in the epigenetic regulator TET2, which lead to clonal hematopoiesis, aggravate age- and obesity-related insulin resistance in mice, and this metabolic dysfunction is paralleled by increased expression of the pro-inflammatory cytokine IL-1β in white adipose tissue, and it is suppressed by pharmacological inhibition of NLRP3 inflammasome-mediated IL- 1β production.

TL;DR: Genetic disruption of p19(ARF) in apoE-null mice augments aortic atherosclerosis without affecting body weight, plasma lipoproteins, or plaque's proliferative activity, and suggest that human genetic variants associated to diminished CDKN2A expression may accelerate Atherosclerosis by limiting plaque apoptosis.

TL;DR: Some mouse models commonly used in studies on ageing are reviewed, the advantages and disadvantages of the different strategies are highlighted, and their relevance to disease susceptibility is discussed.