Study summary · research use only
Mitochondrial stress and mitokines in aging
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses mitokines, signaling molecules including FGF21, GDF15, and mitochondrial-derived peptides such as humanin, that communicate mitochondrial stress between cells and tissues, with responsiveness to stimuli such as exercise in skeletal muscle. The authors summarize mitokine involvement in aging and age-related metabolic, cardiovascular, and neurological diseases, noting mitokine synthesis may increase compensatorily to preserve mitochondrial function, while resistance to mitokine actions may also develop. The review states whether mitokine changes contribute to aging or represent 'rescue factors' remains unresolved, that reduced mitokine levels may impair inter-organ crosstalk, and that excessive mitokine concentrations have been associated with conditions such as cancer and heart failure. Regular exercise is associated with mitokine signaling and increased lifespan in cited literature.
Abstract
Mitokines are signaling molecules that enable communication of local mitochondrial stress to other mitochondria in distant cells and tissues. Among those molecules are FGF21, GDF15 (both expressed in the nucleus) and several mitochondrial-derived peptides, including humanin. Their responsiveness to mitochondrial stress induces mitokine-signaling in response for example to exercise, following mitochondrial challenges in skeletal muscle. Such signaling is emerging as an important mediator of exercise-derived and dietary strategy-related molecular and systemic health benefits, including healthy aging. A compensatory increase in mitokine synthesis and secretion could preserve mitochondrial function and overall cellular vitality. Conversely, resistance against mitokine actions may also develop. Alterations of mitokine-levels, and therefore of mitokine-related inter-tissue cross talk, are associated with general aging processes and could influence the development of age-related chronic metabolic, cardiovascular and neurological diseases; whether these changes contribute to aging or represent "rescue factors" remains to be conclusively shown. The aim of the present review is to summarize the expanding knowledge on mitokines, the potential to modulate them by lifestyle and their involvement in aging and age-related diseases. We highlight the importance of well-balanced mitokine-levels, the preventive and therapeutic properties of maintaining mitokine homeostasis and sensitivity of mitokine signaling but also the risks arising from the dysregulation of mitokines. While reduced mitokine levels may impair inter-organ crosstalk, also excessive mitokine concentrations can have deleterious consequences and are associated with conditions such as cancer and heart failure. Preservation of healthy mitokine signaling levels can be achieved by regular exercise and is associated with an increased lifespan.
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