Mitochondrial Dysfunction in Ageing and Diseases (Record no. 80103)

MARC details
000 -LEADER
fixed length control field 03165naaaa2200349uu 4500
001 - CONTROL NUMBER
control field https://directory.doabooks.org/handle/20.500.12854/53608
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20220220100052.0
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9783038422525
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9783038422518
041 0# - LANGUAGE CODE
Language code of text/sound track or separate title English
042 ## - AUTHENTICATION CODE
Authentication code dc
245 10 - TITLE STATEMENT
Title Mitochondrial Dysfunction in Ageing and Diseases
260 ## - PUBLICATION, DISTRIBUTION, ETC.
Name of publisher, distributor, etc. MDPI - Multidisciplinary Digital Publishing Institute
Date of publication, distribution, etc. 2016
300 ## - PHYSICAL DESCRIPTION
Extent 1 electronic resource (XXVI, 516 p.)
506 0# - RESTRICTIONS ON ACCESS NOTE
Terms governing access Open Access
Source of term star
Standardized terminology for access restriction Unrestricted online access
520 ## - SUMMARY, ETC.
Summary, etc. 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
540 ## - TERMS GOVERNING USE AND REPRODUCTION NOTE
Terms governing use and reproduction Creative Commons
Use and reproduction rights https://creativecommons.org/licenses/by-nc-nd/4.0/
Source of term cc
-- https://creativecommons.org/licenses/by-nc-nd/4.0/
546 ## - LANGUAGE NOTE
Language note English
653 ## - INDEX TERM--UNCONTROLLED
Uncontrolled term neurodegenerative diseases
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Uncontrolled term mitochondrial diseases
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Uncontrolled term pain
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Uncontrolled term metabolic diseases
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Uncontrolled term Ageing
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Uncontrolled term protein homeostasis
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Uncontrolled term cell/retrograde signaling
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Uncontrolled term immune system
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Uncontrolled term cancer
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Uncontrolled term therapies to counteract mitochondrial dysfunction
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Uncontrolled term oxidative stress
856 40 - ELECTRONIC LOCATION AND ACCESS
Host name www.oapen.org
Uniform Resource Identifier <a href="http://www.mdpi.com/books/pdfview/book/217">http://www.mdpi.com/books/pdfview/book/217</a>
Access status 0
Public note DOAB: download the publication
856 40 - ELECTRONIC LOCATION AND ACCESS
Host name www.oapen.org
Uniform Resource Identifier <a href="https://directory.doabooks.org/handle/20.500.12854/53608">https://directory.doabooks.org/handle/20.500.12854/53608</a>
Access status 0
Public note DOAB: description of the publication

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