Inter-tissue communication of mitochondrial stress and metabolic health

Abstract

Mitochondria function as a hub of the cellular metabolic network. Mitochondrial stress is closely associated with aging and a variety of diseases, including neurodegeneration and cancer. Cells autonomously elicit specific stress responses to cope with mitochondrial stress to maintain mitochondrial homeostasis. Interestingly, mitochondrial stress responses may also be induced in a non-autonomous manner in cells or tissues that are not directly experiencing such stress. Such non-autonomous mitochondrial stress responses are mediated by secreted molecules called mitokines. Due to their significant translational potential in improving human metabolic health, there has been a surge in mitokine-focused research. In this review, we summarize the findings regarding inter-tissue communication of mitochondrial stress in animal models. In addition, we discuss the possibility of mitokine-mediated intercellular mitochondrial communication originating from bacterial quorum sensing.

Lipid and glucose metabolism in senescence

“…Lipotoxicity can cause cellular damage, inflammation, insulin resistance, and apoptosis, leading to metabolic disorders and age-related diseases ( 230 ). Moreover, stress can affect the mitochondrial function and autophagy of cells, which are involved in glucose and lipid metabolism ( 231 ). Mitochondria are organelles that produce energy from glucose and fatty acids, while autophagy is the process that degrades damaged or excess cellular components, such as lipids.…”

“…Mitochondria are organelles that produce energy from glucose and fatty acids, while autophagy is the process that degrades damaged or excess cellular components, such as lipids. Stress can induce mitochondrial stress, which is the imbalance between mitochondrial biogenesis and degradation, resulting in mitochondrial dysfunction, oxidative stress, and impaired energy metabolism ( 231 ). Stress can also modulate autophagy, which can have both beneficial and detrimental effects on senescence depending on the stress type and duration.…”