Abstract
The focus of this chapter is the gender differences in mitochondria in cardiovascular disease. There is broad evidence suggesting that some of the gender differences in cardiovascular outcome may be partially related to differences in mitochondrial biology (Ventura–Clapier R, Moulin M, Piquereau J, Lemaire C, Mericskay M, Veksler V, Garnier A, Clin Sci (Lond) 131(9):803–822, 2017)). Mitochondrial disorders are causally affected by mutations in either nuclear or mitochondrial genes involved in the synthesis of respiratory chain subunits or in their posttranslational control. This can be due to mutations of the mtDNA which are transmitted by the mother or mutations in the nuclear DNA. Because natural selection on mitochondria operates only in females, mutations may have had more deleterious effects in males than in females (Ventura–Clapier R, Moulin M, Piquereau J, Lemaire C, Mericskay M, Veksler V, Garnier A, Clin Sci (Lond) 131(9):803–822, 2017; Camara AK, Lesnefsky EJ, Stowe DF. Antioxid Redox Signal 13(3):279–347, 2010). As mitochondrial mutations can affect all tissues, they are responsible for a large panel of pathologies including neuromuscular disorders, encephalopathies, metabolic disorders, cardiomyopathies, neuropathies, renal dysfunction, etc. Many of these pathologies present sex/gender specificity. Thus, alleviating or preventing mitochondrial dysfunction will contribute to mitigating the severity or progression of the development of diseases. Here, we present evidence for the involvement of mitochondria in the sex specificity of cardiovascular disorders.
| Original language | English |
|---|---|
| Title of host publication | Advances in Experimental Medicine and Biology |
| Publisher | Springer New York LLC |
| Pages | 241-256 |
| Number of pages | 16 |
| DOIs | |
| Publication status | Published - Jan 1 2018 |
Publication series
| Name | Advances in Experimental Medicine and Biology |
|---|---|
| Volume | 1065 |
| ISSN (Print) | 0065-2598 |
| ISSN (Electronic) | 2214-8019 |
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Keywords
- Aging heart
- Apoptotic bodies
- Autophagy
- Calcium overload
- Dynamin
- Heart failure
- Ischemic preconditioning
- Krebs cycle
- Mitochondrial biology
- Mitochondrial dysfunction
- Mitophagy
- Mutations of mtDNA
- Nuclear respiratory factor
- Reactive oxygen species
- Redox messenger
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
Mitochondria and sex-specific cardiac function. / Vona, Rosa; Ascione, Barbara; Malorni, Walter; Straface, Elisabetta.
Advances in Experimental Medicine and Biology. Springer New York LLC, 2018. p. 241-256 (Advances in Experimental Medicine and Biology; Vol. 1065).Research output: Chapter in Book/Report/Conference proceeding › Chapter
}
TY - CHAP
T1 - Mitochondria and sex-specific cardiac function
AU - Vona, Rosa
AU - Ascione, Barbara
AU - Malorni, Walter
AU - Straface, Elisabetta
PY - 2018/1/1
Y1 - 2018/1/1
N2 - The focus of this chapter is the gender differences in mitochondria in cardiovascular disease. There is broad evidence suggesting that some of the gender differences in cardiovascular outcome may be partially related to differences in mitochondrial biology (Ventura–Clapier R, Moulin M, Piquereau J, Lemaire C, Mericskay M, Veksler V, Garnier A, Clin Sci (Lond) 131(9):803–822, 2017)). Mitochondrial disorders are causally affected by mutations in either nuclear or mitochondrial genes involved in the synthesis of respiratory chain subunits or in their posttranslational control. This can be due to mutations of the mtDNA which are transmitted by the mother or mutations in the nuclear DNA. Because natural selection on mitochondria operates only in females, mutations may have had more deleterious effects in males than in females (Ventura–Clapier R, Moulin M, Piquereau J, Lemaire C, Mericskay M, Veksler V, Garnier A, Clin Sci (Lond) 131(9):803–822, 2017; Camara AK, Lesnefsky EJ, Stowe DF. Antioxid Redox Signal 13(3):279–347, 2010). As mitochondrial mutations can affect all tissues, they are responsible for a large panel of pathologies including neuromuscular disorders, encephalopathies, metabolic disorders, cardiomyopathies, neuropathies, renal dysfunction, etc. Many of these pathologies present sex/gender specificity. Thus, alleviating or preventing mitochondrial dysfunction will contribute to mitigating the severity or progression of the development of diseases. Here, we present evidence for the involvement of mitochondria in the sex specificity of cardiovascular disorders.
AB - The focus of this chapter is the gender differences in mitochondria in cardiovascular disease. There is broad evidence suggesting that some of the gender differences in cardiovascular outcome may be partially related to differences in mitochondrial biology (Ventura–Clapier R, Moulin M, Piquereau J, Lemaire C, Mericskay M, Veksler V, Garnier A, Clin Sci (Lond) 131(9):803–822, 2017)). Mitochondrial disorders are causally affected by mutations in either nuclear or mitochondrial genes involved in the synthesis of respiratory chain subunits or in their posttranslational control. This can be due to mutations of the mtDNA which are transmitted by the mother or mutations in the nuclear DNA. Because natural selection on mitochondria operates only in females, mutations may have had more deleterious effects in males than in females (Ventura–Clapier R, Moulin M, Piquereau J, Lemaire C, Mericskay M, Veksler V, Garnier A, Clin Sci (Lond) 131(9):803–822, 2017; Camara AK, Lesnefsky EJ, Stowe DF. Antioxid Redox Signal 13(3):279–347, 2010). As mitochondrial mutations can affect all tissues, they are responsible for a large panel of pathologies including neuromuscular disorders, encephalopathies, metabolic disorders, cardiomyopathies, neuropathies, renal dysfunction, etc. Many of these pathologies present sex/gender specificity. Thus, alleviating or preventing mitochondrial dysfunction will contribute to mitigating the severity or progression of the development of diseases. Here, we present evidence for the involvement of mitochondria in the sex specificity of cardiovascular disorders.
KW - Aging heart
KW - Apoptotic bodies
KW - Autophagy
KW - Calcium overload
KW - Dynamin
KW - Heart failure
KW - Ischemic preconditioning
KW - Krebs cycle
KW - Mitochondrial biology
KW - Mitochondrial dysfunction
KW - Mitophagy
KW - Mutations of mtDNA
KW - Nuclear respiratory factor
KW - Reactive oxygen species
KW - Redox messenger
UR - http://www.scopus.com/inward/record.url?scp=85051272142&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85051272142&partnerID=8YFLogxK
U2 - 10.1007/978-3-319-77932-4_16
DO - 10.1007/978-3-319-77932-4_16
M3 - Chapter
C2 - 30051389
AN - SCOPUS:85051272142
T3 - Advances in Experimental Medicine and Biology
SP - 241
EP - 256
BT - Advances in Experimental Medicine and Biology
PB - Springer New York LLC
ER -