BACKGROUND: Mitochondria are widely reported to occupy a unique role in modulating cell viability, senescence and death. This is consistently supported by the multiple functions of these organelles. In addition to providing the energy for the myriad of cellular performances, mitochondria are involved in regulating thermogenesis, calcium buffering, integration of pro- and anti-apoptotic signals. OBJECTIVE: To stress the significant importance of subtle, continuous and permanent mitochondrial alterations as key events in physiological aging and as unfavourable determinants of age-related neurodegenerative diseases. RESULTS: Any dysfunction of these organelles may constitute a serious threat for cellular health status and survival, particularly of post-mitotic nerve and muscle cells. Mitochondrial deterioration may affect discrete features of the organelles (such as their structural dynamics, genetics and physiology) and lead to a progressive functional impairment. CONCLUSIONS: A variety of mitochondrial tasks, while hampering the possibility to recover the organelles' dysfunctions, offer different and reliable opportunities for therapeutic interventions. Copyright 2004 S. Karger AG, Basel
BACKGROUND: Mitochondria are widely reported to occupy a unique role in modulating cell viability, senescence and death. This is consistently supported by the multiple functions of these organelles. In addition to providing the energy for the myriad of cellular performances, mitochondria are involved in regulating thermogenesis, calcium buffering, integration of pro- and anti-apoptotic signals. OBJECTIVE: To stress the significant importance of subtle, continuous and permanent mitochondrial alterations as key events in physiological aging and as unfavourable determinants of age-related neurodegenerative diseases. RESULTS: Any dysfunction of these organelles may constitute a serious threat for cellular health status and survival, particularly of post-mitotic nerve and muscle cells. Mitochondrial deterioration may affect discrete features of the organelles (such as their structural dynamics, genetics and physiology) and lead to a progressive functional impairment. CONCLUSIONS: A variety of mitochondrial tasks, while hampering the possibility to recover the organelles' dysfunctions, offer different and reliable opportunities for therapeutic interventions. Copyright 2004 S. Karger AG, Basel
Authors: Philippa A Jackson; Emma L Wightman; Rachel Veasey; Joanne Forster; Julie Khan; Caroline Saunders; Siobhan Mitchell; Crystal F Haskell-Ramsay; David O Kennedy Journal: Nutrients Date: 2020-07-28 Impact factor: 5.717