Disparate Roles of Mitochondria in Cell Survival and Cell Death: New Insight from the CNS

About this Research Topic

Background

Mitochondria which played a pivotal role in the evolution of eukaryotic organisms are thought to have evolved from a prokaryotic cell, which entered into an endosymbiotic relationship with an ancestral eukaryotic cell. This partnership conferred great benefits to both organisms and allowed them to utilize oxygen in the developing atmosphere. By virtue of its ability to produce ATP, mitochondria are the powerhouse of the cell and are indispensable to the survival of most eukaryotic organisms. Paradoxically, the same organelle plays a crucial role in orchestrating programmed cell death in cells. This occurs by several interrelated mechanisms including: 1) Compromise of mitochondrial bioenergetics and a subsequent decline in ATP production, 2) Release of mitochondrial proteins such as cytochrome c into the cytosol and/or, 3) Changes in the redox potential of the cell. In the 1990s, there was a profusion of publications addressing detailed mitochondrial mechanisms contributing to cell death via the caspase family of proteases and the role of Bcl2 family of proteins that acted as either pro- or anti-apoptotic agents influencing cell death. However, the detailed mechanisms by which mitochondria contribute to cell death are still not completely understood.

The CNS including the retina has high energy requirements and oxygen consumption, hence is characterized by an abundance of mitochondria. While mitochondria are present in all tissues in the body, the impact of mitochondrial gene mutations is felt mainly in the retina, optic nerve and brain and exemplified by conditions such as Dominant optic Atrophy, Leber’s Hereditary Optic Neuropathy and Leigh syndrome. In addition, mitochondrial dysfunction is implicated in several neurodegenerative diseases, including glaucoma, age-related macular degeneration (AMD), Parkinson’s and Alzheimer’s disease. This has evoked great interest in mitochondrial pathways contributing to the etiology of these diseases. In recent years mitochondrial research has taken new directions including mechanisms of mitochondrial dynamics, fusion and fission. By constant fusion and fission, mitochondria form a network that is modified according to the needs of the cell. Excessive fission has been shown to be damaging to cells and associated with ageing and neurodegeneration. Damaged mitochondria are enclosed by a double-membraned structure called phagophore which mature into autophagosome/mitophagosome that fuse with lysosome to target the mitochondria for degradation.

This process is important as a quality control mechanism of mitochondria for cells to retain healthy mitochondria, which in turn is necessary for optimum health of the tissue and organism. A decline in mitophagy has been reported to contribute to neurodegenerative diseases. In an exciting development, mitochondrial transplantation is emerging as a new avenue to replace damaged mitochondria in pathologies of CNS. The research topic will focus on mitochondrial mechanisms including mitochondrial dynamics, bioenergetics, and mitophagy, which influence cell survival and cell death pathways, consequently having an effect on normal health and disease pathologies of the CNS.

Keywords: Mitochondria, Optic Neurodegeneration

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