Katerina I. Leonova

TL;DR: Old mice with elevated proportion of p16(Ink4a)/β-galpH6-positive cells in their tissues demonstrated reduction of both following systemic clodronate treatment, indicating that a significant proportion of cells previously considered to be SCs are actually a subclass of macrophages.

TL;DR: It is reported that SIRT6-deficient cells and tissues accumulate abundant cytoplasmic L1 cDNA, which triggers strong type I interferon response via activation of cGAS, and modulating L1 activity may be an important strategy for attenuating age-related pathologies.

TL;DR: It is shown that the tumor suppressor protein p53 cooperates with DNA methylation to maintain silencing of a large portion of the mouse genome, and roles for p53 and IFN that are key for genetic stability and therefore relevant to both tumorigenesis and the evolution of species are revealed.

TL;DR: It is reported that expression of p 16Ink4a and SAβG in macrophages is acquired as part of a physiological response to immune stimuli rather than through senescence, consistent with reports that p16InK4a plays a role in Macrophage polarization and response.

TL;DR: It is demonstrated that Klf9 independently causes increased ROS levels in various types of cultured cells and in mouse tissues and is required for pathogenesis of bleomycin-induced pulmonary fibrosis in mice and identified as a ubiquitous regulator of oxidative stress and lung injury.