| 000 | 03165naaaa2200349uu 4500 | ||
|---|---|---|---|
| 001 | https://directory.doabooks.org/handle/20.500.12854/53608 | ||
| 005 | 20220220100052.0 | ||
| 020 | _a9783038422525 | ||
| 020 | _a9783038422518 | ||
| 041 | 0 | _aEnglish | |
| 042 | _adc | ||
| 245 | 1 | 0 | _aMitochondrial Dysfunction in Ageing and Diseases |
| 260 |
_bMDPI - Multidisciplinary Digital Publishing Institute _c2016 |
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| 300 | _a1 electronic resource (XXVI, 516 p.) | ||
| 506 | 0 |
_aOpen Access _2star _fUnrestricted online access |
|
| 520 | _aThe 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 |
_aCreative Commons _fhttps://creativecommons.org/licenses/by-nc-nd/4.0/ _2cc _4https://creativecommons.org/licenses/by-nc-nd/4.0/ |
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| 546 | _aEnglish | ||
| 653 | _aneurodegenerative diseases | ||
| 653 | _amitochondrial diseases | ||
| 653 | _apain | ||
| 653 | _ametabolic diseases | ||
| 653 | _aAgeing | ||
| 653 | _aprotein homeostasis | ||
| 653 | _acell/retrograde signaling | ||
| 653 | _aimmune system | ||
| 653 | _acancer | ||
| 653 | _atherapies to counteract mitochondrial dysfunction | ||
| 653 | _aoxidative stress | ||
| 856 | 4 | 0 |
_awww.oapen.org _uhttp://www.mdpi.com/books/pdfview/book/217 _70 _zDOAB: download the publication |
| 856 | 4 | 0 |
_awww.oapen.org _uhttps://directory.doabooks.org/handle/20.500.12854/53608 _70 _zDOAB: description of the publication |
| 999 |
_c80103 _d80103 |
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