Jeanne Mialet-Perez, Angers University

Abstract 

Heart failure (HF) is the leading cause of hospitalization and death in subjects over 60 and its prevalence is constantly increasing due to the aging of the population. Understanding the molecular mechanisms that underlie the development of HF represents a major economical and societal challenge. In this context, our work has focused on particular signaling pathways in the heart related to reactive oxygen species (ROS), mitochondrial dysfunction, telomere damage and their involvement in senescence, a cellular process closely linked to aging. We discovered for the first time the role of monoamine oxidase-A (MAO-A) and its mechanisms of action in HF and aging. In addition, we identified non-canonical mechanisms of post-mitotic senescence of cardiomyocytes, with relevance not only in cardiac aging but also in post-ischemic remodeling. Our most recent study focuses on the newly identified role of mitochondria in the release of mitochondrial DNA and activation of inflammatory pathways in the heart. Altogether, our work put forward the role of mitochondrial dysfunction in deleterious cellular processes leading to cardiac aging that could offer new senotherapeutic strategies for HF.

Biography

Jeanne Mialet-Perez is permanent researcher at INSERM-CNRS Institute “Mitovasc” in Angers, France. She received her Ph.D. degree from the University of Paris-Saclay in 2002, followed by a postdoctoral training at the University of Cincinnati on the genetic variants of adrenergic receptors and their functional impacts in cardiac diseases. Back at I2MC in Toulouse, France, she contributed to uncover the role of cardiac monoamine oxidases, the mitochondrial enzymes that degrade catecholamines and serotonin, in the generation of deleterious ROS and aldehydes in age-associated diseases such as heart failure. In the meantime, she contributed to the description and understanding of the mechanisms involved in cardiomyocyte and stromal cell senescence in the aging heart. She is currently focusing her research at Mitolab in Angers on gaining a deeper understanding of the complex relationship between mitochondrial dysfunction and senescence. For this purpose, she studies specific signaling pathways leading to senescence in vitro and in pre-clinical models of chronic cardiac diseases and mitochondrial genetic diseases.