Dr Satomi Miwa; Newcastle University
I was originally a sport scientist and became interested in energy metabolism, mitochondria and oxidative stress. Following my PhD on mitochondrial reactive oxygen species (ROS) production and ageing in Cambridge University, my research interests have been centred around the roles of mitochondrial function in ageing, cell senescence and diseases. One example of my recent work is on senescent cell targeted therapies that involve manipulation of mitochondrial function, and we investigate novel approaches both in vitro and preclinical in vivo settings. To further explore fundamental mechanism of ageing, my recent research aims to ask how stress response mechanisms, which are necessary to maintain physiological homeostasis during various challenges brought environmentally or endogenously, regulate ageing. Our hypothesis is that sex specific stress response may contribute the sex differences in ageing. Apart from research, I lead the Biology of Ageing Special Interest Group (SIG) at Newcastle University, and act as the Newcastle lead for international ageing research networks, including H2020 teaming programme MIA Portugal, and the Alliance for Healthy Aging. I am also the programme lead for MRes Ageing and Health and the Biology of Ageing module at Newcastle University.
Hormesis, the adaptive activation of cytoprotective stress-response pathways by subtoxic or metabolic challenges, provides a mechanistic framework for numerous longevity interventions. Regimens such as dietary restriction and several pharmacological agents are hypothesised to exert their lifespan- and healthspan-extending effects, at least in part, through hormetic mechanisms that enhance stress resistance and physiological resilience. Regulatory long-term toxicity studies submitted to national and international agencies represent an underexploited source of high-quality survival data in rodents, as their archives contain datasets amenable to secondary analysis, potentially revealing compounds that paradoxically confer survival benefits. We interrogated the electronic Archive of Studies and Assessments of the German Federal Institute for Risk Assessment, which encompasses plant protection and biocidal products (pesticides). Our analysis identified 27 substances (18% of sampled entries) associated with increased survival at least 10% at study termination (p < 0.05). We found that approximately half of the disclosed compounds perturbed mammalian mitochondrial function, implicating mitochondrial stress responses as candidate mechanisms mediating enhanced survival in mammals. At the cellular level, senescence constitutes a fundamental stress response. While transient senescence is indispensable for processes such as morphogenesis and tissue repair, persistent senescent cells contribute causally to age-related pathologies. We hypothesise that sex differences in ageing, characterised by females’ greater life expectancy yet paradoxically earlier onset of inflammatory and pathological conditions, may be explained by differential stress-response capacity, predisposing females to higher senescence burden, while offering survival resilience. This seminar will examine whether sex-specific variation in stress responses and senescence dynamics underlies these phenomena, drawing on recent experimental data from our laboratory.
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