Mitochondrial Dysfunction in Ageing and Diseases

The past decade has witnessed an explosion of knowledge regarding how mitochondrial dysfunction may translate into ageing and disease phenotypes, as well as how it is modulated by genetic and lifestyle factors. Impairment of the mitochondria may be caused by mutations or deletions in nuclear or mito...

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Publicado: MDPI - Multidisciplinary Digital Publishing Institute 2021
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collection Directory of Open Access Books
description The past decade has witnessed an explosion of knowledge regarding how mitochondrial dysfunction may translate into ageing and disease phenotypes, as well as how it is modulated by genetic and lifestyle factors. Impairment of the mitochondria may be caused by mutations or deletions in nuclear or mitochondrial DNA. Hallmarks of mitochondrial dysfunction include decreased ATP production, decreased mitochondrial membrane potential, swollen mitochondria, damaged cristae, increased oxidative stress, and decreased mitochondrial DNA copy number. In addition to energy production, mitochondria play an important role in regulating apoptosis, buffering calcium release, retrograde signaling to the nuclear genome, producing reactive oxygen species (ROS), participating in steroid synthesis, signaling to the immune system, as well as controlling the cell cycle and cell growth. Dysfunctional mitochondria have been implicated in ageing and in several diseases, many of which are age-related, including mitochondrial diseases, cancers, metabolic diseases and diabetes, inflammatory conditions, neuropathy, and neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease. Additionally, a possible link between mitochondrial metabolism and the ubiquitin-proteasome and autophagy-lysosome systems is emerging as a novel factor contributing to the progression of several human diseases. This special issue calls for original research, mini and full reviews, and perspectives that address the progress and current standing in the vast field of mitochondrial biology. These include, but are not limited to: ageing neurodegenerative diseases mitochondrial diseases metabolic diseases protein homeostasis cell/retrograde signaling oxidative stress pain cancer immune system therapies to counteract mitochondrial dysfunction
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spelling doab-20.500.12854ir-536082022-01-31T12:14:53Z Mitochondrial Dysfunction in Ageing and Diseases neurodegenerative diseases mitochondrial diseases pain metabolic diseases Ageing protein homeostasis cell/retrograde signaling immune system cancer therapies to counteract mitochondrial dysfunction oxidative stress The past decade has witnessed an explosion of knowledge regarding how mitochondrial dysfunction may translate into ageing and disease phenotypes, as well as how it is modulated by genetic and lifestyle factors. Impairment of the mitochondria may be caused by mutations or deletions in nuclear or mitochondrial DNA. Hallmarks of mitochondrial dysfunction include decreased ATP production, decreased mitochondrial membrane potential, swollen mitochondria, damaged cristae, increased oxidative stress, and decreased mitochondrial DNA copy number. In addition to energy production, mitochondria play an important role in regulating apoptosis, buffering calcium release, retrograde signaling to the nuclear genome, producing reactive oxygen species (ROS), participating in steroid synthesis, signaling to the immune system, as well as controlling the cell cycle and cell growth. Dysfunctional mitochondria have been implicated in ageing and in several diseases, many of which are age-related, including mitochondrial diseases, cancers, metabolic diseases and diabetes, inflammatory conditions, neuropathy, and neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease. Additionally, a possible link between mitochondrial metabolism and the ubiquitin-proteasome and autophagy-lysosome systems is emerging as a novel factor contributing to the progression of several human diseases. This special issue calls for original research, mini and full reviews, and perspectives that address the progress and current standing in the vast field of mitochondrial biology. These include, but are not limited to: ageing neurodegenerative diseases mitochondrial diseases metabolic diseases protein homeostasis cell/retrograde signaling oxidative stress pain cancer immune system therapies to counteract mitochondrial dysfunction 2021-02-11T19:47:59Z 2021-02-11T19:47:59Z 2016-08-16 07:37:51 2016 book 19508 9783038422525 9783038422518 https://directory.doabooks.org/handle/20.500.12854/53608 eng application/octet-stream Attribution-NonCommercial-NoDerivatives 4.0 International http://amzn.to/2bmNiFS http://www.mdpi.com/books/pdfview/book/217 MDPI - Multidisciplinary Digital Publishing Institute 46cabcaa-dd94-4bfe-87b4-55023c1b36d0 9783038422525 9783038422518 XXVI, 516 open access
spellingShingle neurodegenerative diseases
mitochondrial diseases
pain
metabolic diseases
Ageing
protein homeostasis
cell/retrograde signaling
immune system
cancer
therapies to counteract mitochondrial dysfunction
oxidative stress
Mitochondrial Dysfunction in Ageing and Diseases
title Mitochondrial Dysfunction in Ageing and Diseases
title_full Mitochondrial Dysfunction in Ageing and Diseases
title_fullStr Mitochondrial Dysfunction in Ageing and Diseases
title_full_unstemmed Mitochondrial Dysfunction in Ageing and Diseases
title_short Mitochondrial Dysfunction in Ageing and Diseases
title_sort mitochondrial dysfunction in ageing and diseases
topic neurodegenerative diseases
mitochondrial diseases
pain
metabolic diseases
Ageing
protein homeostasis
cell/retrograde signaling
immune system
cancer
therapies to counteract mitochondrial dysfunction
oxidative stress
topic_facet neurodegenerative diseases
mitochondrial diseases
pain
metabolic diseases
Ageing
protein homeostasis
cell/retrograde signaling
immune system
cancer
therapies to counteract mitochondrial dysfunction
oxidative stress
url 19508