Abstract
Recent studies have revealed that some low-molecular weight molecules produced in mitochondria are essential contributing factors to aging and aging-associated pathologies in evolutionarily distant eukaryotes. These molecules are intermediates or products of certain metabolic reactions that are activated in mitochondria in response to specific changes in the nutrient, stress, proliferation, or age status of the cell. After being released from mitochondria, these metabolites directly or indirectly change activities of a distinct set of protein sensors that reside in various cellular locations outside of mitochondria. Because these protein sensors control the efficiencies of some pro- or anti-aging cellular processes, such changes in their activities allow to create a pro- or anti-aging cellular pattern. Thus, mitochondria can function as signaling platforms that respond to certain changes in cell stress and physiology by remodeling their metabolism and releasing a specific set of metabolites known as “mitobolites.” These mitobolites then define the pace of cellular and organismal aging because they regulate some longevity-defining processes taking place outside of mitochondria. In this review, we discuss recent progress in understanding mechanisms underlying the ability of mitochondria to function as such signaling platforms in aging and aging-associated diseases.
Highlights
Because mitochondria generate the bulk of cellular ATP, the functional state of these organelles is essential for physiology of all eukaryotic organisms (Nunnari and Suomalainen, 2012)
Mitochondria can respond to changes in the nutrient, Mitochondria-Generated Metabolites in Aging stress, proliferation or age status of the cell by altering the rates of catabolic and anabolic reactions yielding many different metabolites (Green et al, 2011; Nunnari and Suomalainen, 2012; López-Otín et al, 2013)
A body of recent evidence indicates that some of these mitochondria-generated metabolites can function as second messengers whose concentrations regulate longevity-defining processes in various cellular locations, thereby contributing to cellular and organismal aging (Leonov and Titorenko, 2013; Chandel, 2014; Beach et al, 2015; Quirós et al, 2016; Matilainen et al, 2017)
Summary
Because mitochondria generate the bulk of cellular ATP, the functional state of these organelles is essential for physiology of all eukaryotic organisms (Nunnari and Suomalainen, 2012).
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