Abstract
Aging is an important and inevitable biological process in human life, associated with the onset of chronic disease and death. The mechanisms behind aging remain unclear. However, changes in mitochondrial function and structure, including reduced activity of the mitochondrial respiratory chain and increased production of reactive oxygen species—thus oxidative damage—are believed to play a major role. Mitochondria are the main source of cellular energy, producing adenosine triphosphate (ATP) via oxidative phosphorylation. Accumulation of damaged cellular components reduces a body's capacity to preserve tissue homeostasis and affects biological aging and all age-related chronic conditions. This includes the onset and progression of classic degenerative diseases such as cardiovascular disease, kidney failure, neurodegenerative diseases, and cancer. Clinical manifestations of intestinal disorders, such as mucosal barrier dysfunction, intestinal dysmotility, and chronic obstipation, are highly prevalent in the elderly population and have been shown to be associated with an age-dependent decline of mitochondrial function. This review summarizes our current understanding of the role of mitochondrial dysfunction in intestinal aging.
Highlights
Mitochondria are double-membrane organelles that contain their own circular double-stranded DNA [1, 2]
Mitochondria are composed of four compartments: (a) the mitochondrial matrix containing the mitochondrial genome, its transcription and translation machinery, and enzymes involved in β-oxidation and the citric acid-cycle; (b) the inner membrane and its embedded oxidative phosphorylation (OXPHOS) complexes which generate adenosine triphosphate (ATP) for cellular processes; (c) the outer membrane containing proteins involved in cell death and protein import as well as voltage-dependent anion channels (VDAC); and (d) the intermembrane space housing intermediate products of OXPHOS [3, 38]
Aging is associated with a decline in energy production at the cellular level caused by mitochondrial alterations
Summary
Mitochondria are double-membrane organelles that contain their own circular double-stranded DNA (mtDNA) [1, 2]. They convert carbohydrates and fats, which are the main sources of cellular energy, into adenosine triphosphate (ATP) by oxidative phosphorylation (OXPHOS) via the mitochondrial respiratory chain (RC). Accumulation of damaged cellular components causes a decline in physiological function and a reduced capacity to maintain tissue homeostasis, which plays a pivotal role in the process of aging [1, 14,15,16,17].
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