Mitochondrial form, function and signalling in aging

Abstract

Aging is often accompanied by a decline in mitochondrial mass and function in different tissues. Additionally, cell resistance to stress is frequently found to be prevented by higher mitochondrial respiratory capacity. These correlations strongly suggest mitochondria are key players in aging and senescence, acting by regulating energy homeostasis, redox balance and signalling pathways central in these processes. However, mitochondria display a wide array of functions and signalling properties, and the roles of these different characteristics are still widely unexplored. Furthermore, differences in mitochondrial properties and responses between tissues and cell types, and how these affect whole body metabolism are also still poorly understood. This review uncovers aspects of mitochondrial biology that have an impact upon aging in model organisms and selected mammalian cells and tissues.

Plasma serotonin levels are associated with antidepressant response to SSRIs

“…Certain processes have been proposed as contributing to the risk for these somatic diseases, including accelerated biological aging [45-56], sympathetic and glucocorticoid dysregulation [43, 57-61], metabolic changes [41, 45, 62, 63], inflammation [43, 57, 58, 64-71] and others. Some of these processes may involve changes in energy balance and mitochondrial function [72][73][74][75][76][77] that may be revealed by changes in metabolomic profiles.…”

Mitochondrial dysfunction in neurodegenerative diseases and the potential countermeasure

“…Aging induces many potentially interconnected defects and is a common risk factor for adult human diseases. During the aging process, multiple mitochondrial anomalies may occur, including bioenergetic deficiency, the increased oxidative stress from respiratory chain, and the accumulation of the dysfunctional mitochondria . Damaged mitochondrial DNA (mtDNA) and the accumulation of injured mitochondria are considered major contributors to aging.…”

Synergism and antagonism of two distinct, but confused, Nrf1 factors in integral regulation of the nuclear-to-mitochondrial respiratory and antioxidant transcription networks

“…Amongst them, the mitochondrion is known as a central site of cellular respiration, redox metabolism and biosynthesis, in order to meet a host of energy and growth demands (3,4).…”

“…Thereby, this organelle has its own genetic system with the bacteria-like features, including a compact circular mtDNA genome (from maternal inheritance), along with a simple transcription system that yields multigenic RNA transcripts, and a translational apparatus with similar antibiotic sensitivities to prokaryotic cells. During subsequent endosymbiotic evolution, most of mitochondrial original genes have been lost or transferred to the nucleus in the eukaryotic cells, so that only 37 genes are retained in mammalian mitochondria (3,5). In this genome, only 13 mitochondrial genes encode proteins as essential subunits of the respiratory chain, whilst the remaining 24 genes encode specific tRNA and rRNA required for its protein translation within the mitochondrial matrix (8,9).…”