Redox control of senescence and age-related disease

The signaling networks that drive the aging process, associated functional deterioration, and pathologies has captured the scientific community's attention for decades. While many theories exist to explain the aging process, the production of reactive oxygen species (ROS) provides a signaling link between engagement of cellular senescence and several age-associated pathologies. Cellular senescence has evolved to restrict tumor progression but the accompanying senescence-associated secretory phenotype (SASP) promotes pathogenic pathways. Here, we review known biological theories of aging and how ROS mechanistically control senescence and the aging process. We also describe the redox-regulated signaling networks controlling the SASP and its important role in driving age-related diseases. Finally, we discuss progress in designing therapeutic strategies that manipulate the cellular redox environment to restrict age-associated pathology. Keywords: Oxidative stress, Aging, Senescence, Senescence-associated secretory phenotype (SASP), Reactive oxygen species (ROS

Aproximación al fenómeno del paro: Un modelo explicativo

Se hacen algunas reflexiones sustantivas y metodológicas referentes al estudio del fenómeno del desempleo y de sus efectos psicológicos sobre el individuo. A continuación se propone un modelo teórico explicativo, caracterizado como racional, positivista, y capaz de proporcionar una comprensión mejor de la realidad y de conducir hacia soluciones alternativas. El modelo considera tres niveles: la realidad social como conjunto; la realidad resultante a partir del filtro de la situación laboral; y la situación concreta de los individuos

Redox-control of the alarmin, Interleukin-1α

The pro-inflammatory cytokine Interleukin-1α (IL-1α) has recently emerged as a susceptibility marker for a wide array of inflammatory diseases associated with oxidative stress including Alzheimer's, arthritis, atherosclerosis, diabetes and cancer. In the present study, we establish that expression and nuclear localization of IL-1α are redox-dependent. Shifts in steady-state H2O2 concentrations (SS-[H2O2]) resulting from enforced expression of manganese superoxide dismutase (SOD2) drive IL-1α mRNA and protein expression. The redox-dependent expression of IL-1α is accompanied by its increased nuclear localization. Both IL-1α expression and its nuclear residency are abrogated by catalase co-expression. Sub-lethal doses of H2O2 also cause IL-1α nuclear localization. Mutagenesis revealed IL-1α nuclear localization does not involve oxidation of cysteines within its N terminal domain. Inhibition of the processing enzyme calpain prevents IL-1α nuclear localization even in the presence of H2O2. H2O2 treatment caused extracellular Ca2+ influx suggesting oxidants may influence calpain activity indirectly through extracellular Ca2+ mobilization. Functionally, as a result of its nuclear activity, IL-1α overexpression promotes NF-kB activity, but also interacts with the histone acetyl transferase (HAT) p300. Together, these findings demonstrate a mechanism by which oxidants impact inflammation through IL-1α and suggest that antioxidant-based therapies may prove useful in limiting inflammatory disease progression

Libro Digital Proyectos Posgrados 2015-30

MaestríaDoctoradoDoctor en Ingeniería Eléctrica y ElectrónicaDoctor en Ingeniería CivilDoctor en Ingeniería de Sistemas y ComputaciónDoctor en Ingeniería IndustrialDoctor en Ingeniería MecánicaMagister en Gobierno de Tecnología InformáticaMagister en Ingeniería AdministrativaMagister en Ingeniería AmbientalMagister en Ingeniería CivilMagister en Ingeniería de Sistemas y ComputaciónMagister en Ingeniería EléctricaMagister en Ingeniería ElectrónicaMagister en Ingeniería IndustrialMagister en Ingeniería Mecánic

Delaying surgery for patients with a previous SARS-CoV-2 infection

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